Case Study (Heart Failure)

Case Study (Heart Failure)
Case Study 1 Heart Failure M.G., a "frequent flier," is admitted to the emergency department (ED) with a diagnosis of heart failure (HF). She was
discharged from the hospital 10 days ago and comes in today stating, "I just had to come to the hospital today because I can't catch my breath and
my legs are as big as tree trunks." After further questioning, you learn she is strictly following the fluid and salt restriction ordered during her last
hospital admission. She reports gaining 1 to 2 pounds every day since her discharge. 1. What error in teaching most likely occurred when M.G. was
discharged 10 days ago? If M.G. is currently following her fluid and salt restriction strictly but is still exhibiting the symptoms of fluid... Show more
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What is the rationale for changing the route of the furosemide (Lasix)? The medication will work quicker via the IVP route because it is available
to the bloodstream much quicker than with the oral route, this will allow M.G. to start losing the excess fluid that is causing her unwanted
symptoms. 5. You administer furosemide (Lasix) 80mg IVP. Identify three parameters you would use to monitor the effectiveness of this medication.
The three parameters to check for effectiveness of the furosemide would be: urine output, lung sounds (no crackles) and daily weights. 6. What
laboratory tests should be ordered for M.G. related to the order for furosemide (Lasix)? (Select all that apply) a. Magnesium level b. Sodium level c.
Complete blood count (CBC) d. Serum glucose levels e. Potassium level f. Coagulation studies 7. What is the purpose of the beta blocker carvedilol?
It is given to: g. Increase the contractility of the heart h. Cause peripheral dilation i. Increase urine output j. Reduce cardiac stimulation by
catecholamines Case Study
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Reference Guide for Pharmacy Technician Exam Essay
Reference Guide for Pharmacy Technician Exam
Krisman
REFERENCE GUIDE
FOR PHARMACY
TECHNICIAN EXAM
EDITION 2014–2015
(Covers an updated 2013–PTCB Blue Print)
MANAN SHROFF
www.pharmacyexam.com
1
Reference Guide for Pharmacy Technician Exam
Krisman
This reference guide is not intended as a substitute for the advice of a physician. Students or readers must consult their physicians about any existing
problem. Do not use any information in this reference guide for any kind of self treatment. Do not administer any dose of mentioned drugs in this
reference guide without consulting your physician. This is only a review guide for preparation for the pharmacy technician board exam. The author of
this reference guide ... Show more content on Helpwriting.net ...
Thrombocytopenia: A low platelets count inblood.
Ventricular arrhythmia: Irregular movements of left ventricles of the heart.
2–ANTIARRHYTHMIC AGENTS

M/A: This class of agents is indicated for the treatment of an irregular heart rhythm.
Brand
Generic
Cordarone
Amiodarone
Norpace
Disopyramide
dry

Most Common Treatments For Heart Failure
One of the most common treatments for heart failure is ACE inhibitors. ACE inhibitors have shown to slow down the course of heart failure and
decrease cardiovascular mortality (1). Overall, they work by suppressing the activity of angiotensin II. ACE inhibitors prevent the conversion of
angiotensin I to angiotensin II by competitively inhibiting the activity of the angiotensin converting enzyme. Since angiotensin II is a vasoconstrictor,
the lack of the protein allows blood vessels to remain dilated which decreases blood pressure. In addition, the lack of angiotensin II decreases
aldosterone release which further lowers the blood pressure and puts less strain on the heart. Angiotensin II has been shown to be involved in the
myocardial ... Show more content on Helpwriting.net ...
In addition, the mass of viable myocardium in the treated participants increased relative to the control group. These results indicate that treatment with
CDCs was somehow able to shrink the scar tissue and stimulate the growth of myocardial tissue. However, the partial regeneration at the affected
regions did not necessarily translate to improved heart function. The ejection fraction of the treatment group only increased from 39% to 41%. It was
theorized that the introduced CDCs activated endogenous regenerative pathways through physical contact and the release of paracrine factors.
Proposed Therapy:
It was originally believed that cardiac stem cells can be transplanted into the infarcted region of a failing heart so that they can proliferate and
differentiate into cardiomyocytes to improve the heart's ability to pump blood. While transplanted cardiac stem cells were shown improve cardiac
function in animal trials and clinical trials, it was later discovered that they did so with the release of paracrine factors, not through differentiation. As
a result, interest in the use of paracrine factors to promote endogenous cardiac regeneration has increased. A proposed therapy to take advantage of the
regenerative properties of paracrine factors is to upregulate, through genetic engineering, a cardiac stem cell's release of factors SCF and IGF–1.
Both IGF–1 and SCF have shown to be potentially useful for heart

Potential Health Risks from Inappropriate Prescription of...
Learning Goals
1) Locate where in the renin–angiotensin–aldosterone pathway ACE inhibitors act
2) Identify commonly prescribed antihypertensive medication by primary care physicians
3) List 3 possible side effects from inappropriate ACE inhibitor prescription
4) Suggest possible regulations of ACE inhibitor use for primary care physicians and alternative treatment plans for patients
Introduction
Cardiac related diseases account for over 56 million annual deaths worldwide.1 Cardiovascular disease (CVD) is the leading cause of death in
economically developed countries and is increasing in occurrence in developing nations.1 The prevalence of CVD increases with age.1 The mean
level of blood pressure, used to diagnose CVD, is higher in ... Show more content on Helpwriting.net ...
She has been smoking a pack of cigarettes per day for the past 20 years. She has admitted to occasional alcohol use. She is allergic to the commonly
prescribed antibiotic penicillin.
Biochemical Mechanisms of ACE Inhibitors
The renin–angiotensin–aldosterone system (RAAS) is a group of hormones that are produced sequentially in order to regulate salt–water homeostasis as
well as blood pressure.5 The first enzyme, renin, is produced by the juxtaglomerular cells of the kidney when blood volume is low and is released into
the bloodstream.3,5,6 Renin then catalyzes the conversion of angiotensinogen to angiotensin I.3,5,6 Angiotensin–converting enzyme (ACE), which is
produced in the lungs, subsequently converts angiotensin I to angiotensin II, a more active enzyme.3,5,6 Angiotensin II has several functions. The
hormone's primary mechanism for increasing blood pressure is through the stimulation of blood vessel constriction. Furthermore, angiotensin II
increases the contractility of the heart via sympathetic activation. It also stimulates anti–diuretic hormone (ADH) release, which increases water
reabsorption at the collecting ducts, resulting

Physiology Test 3 : Hemorrhagic Shock
Majriha Naorin
Physiology Test 3: Hemorrhagic Shock
Introduction
Hypovolemic shock "is an emergency condition in which severe blood and fluid loss make the heart unable to pump enough blood to the body" (
Heller). Hypovolemic shock can be a result of numerous things such as dehydration, excessive diarrhea or bleeding (Nall). Excessive bleeding, both
externally and internally, due to injuries is known as Hemorrhagic shock. Hemorrhagic shock is a type of hypovolemic shock that is "associated with
the sudden and rapid loss of significant amounts of blood" (Dictionary).
Mechanisms of Hemorrhagic Shock
An average person has about five liters of blood in their body. However, if a person starts to lose a massive amount of blood due to severe... Show more
When there is insufficient amount of blood due to blood loss, organs do not obtain the amount of blood that is needed. As a result, the organs do not
receive enough nutrients and oxygen; hypoxia. A decrease of blood pressure also decreases in perfusion of the carotid and aortic bodies, "several
clusters of chemoreceptors" (Boron).This decline in perfusion, increases the rate of the chemoreceptors which increases the firing of the sympathetic
vasoconstriction (Boron).
This activation of the sympathetic nerves causes the release of norepinephrine (neurotransmitters) and epinephrine (hormones) from the adrenal
medulla (located on top of the kidney), which then binds with О±1–adrenoceptors (Klabunde). As a result, the smooth muscle activates and
vasoconstrict. This causes the heart rate to increase along with the stroke volume and total peripheral resistance which prevents blood from escaping.
Due to the increase of heart rate, the hemorrhagic patients will experience tachycardia (Boron).
Though turning on the sympathetic nervous system is body's response to the blood loss so that it can go back to homeostasis, it can also detrimental
to the body. Since there is a severe amount of blood that is exiting the body, by increasing the heart rate, it will be supplying more blood to the wound,
releasing even more blood out of the body. Although the body does not redistribute blood to organs due

Sleep Disturbance And Day Time Sleepiness
which his characterized by snoring, sleep disturbance and day time sleepiness. There is a close relation between OSA and hypertension; as many as
one–third of hypertensive patients and above 80% of those with resistant hypertension have OSA.
Alcohol– Higher intake of alcohol increases the blood pressure. Reducing alcohol leads to fall in the systolic blood pressure.
Stress– Psychological or environmental stress play a part in the causes of hypertension. Direct effects of situations such as poverty, unemployment and
poor education (stressors) are involved, as are other aspects of lifestyle that are linked to hypertension.
Exercise– Physical activity increases blood pressure, but people who exercise regularly have lower blood pressures. Such people, however, also may
have a healthier diet and more sensible drinking and smoking habits.
Other dietary factors– Vegetarians generally have lower BP than non–vegetarians. Reducing a meat rich diet with vegetable products reduces blood
pressure. Caffeine and caffeinated drinks also increases blood pressure and must be avoided.
THE VARIOUS BODY MECHANISMS THAT CAUSES AND INFLUENCES HYPERTENSION
The various mechanisms that cause and influences hypertension are actually built into us for good reasons: we need them to keep our blood pressure
from falling too low. But when they go somewhat awry, they cause high blood pressure. And when that happens, we need treatment for hypertension,
ironically aimed at the same mechanisms.
1. How

Oral And Recurrent Pregnancy Loss
Association between Angiotensin Converting Enzyme Insertion/Deletion (I/D) Polymorphism and Recurrent Pregnancy Loss
Aisha Mahmood Fageer, Elshazali Widaa Ali, Nasr Eldeen Ali Mohamed
Department of haematology, Faculty of medical laboratory sciences, Al Neelain University, Khartoum, Sudan
Corresponding author: Dr. Elshazali Widaa Ali Mohamed Ahmed, Ph.D
Faculty of medical laboratory sciences, Al Neelain University, Khartoum, Sudan
Mobile: 00249122694501, E–mail: elshazaliwidaa@gmail.com
Abstract
Background: Recurrent abortion or recurrent pregnant loss (RPL) is a common clinical problem, and for most women the cause is unknown.
Angiotensin–converting enzyme (ACE) affects vascular structure and placental function, and its role in blood pressure regulation and electrolyte
balance is well documented, as well as it is play a role in regulation of fibrinolysis indirectly.
Objective: This study aimed to examine the association of the ACE I/D polymorphism with recurrent pregnancy loss in Sudanese women.
Materials and methods: It is a case–control study, in which 40 patients with RPL and 40 healthy women with one or more successful pregnancies
were enrolled. Salting out method was used for DNA isolation from peripheral blood leukocytes, and PCR was used to determine the ACE genotypes
(DD, ID, and II).
Results: In women with RPL the frequencies of ACE genotypes were found to be 57.5% for DD, 35.0% for ID, and 7.5% for II. in the control group
the frequencies were 92.5% for DD,

The Physiological Effect Of Angiotensin Renin System
During my undergraduate years, I came across a drug class called Angiotensin Converting Enzyme (ACE) inhibitor. This medicine interferes in a
production of angiotensin II via the enzyme inhibition, ultimately lowering the blood pressure. Understanding the physiological effect of
angiotensin–renin system greatly fascinated me how our body is sophisticated in its structure and function, and it intrigued me further that our current
knowledge allows us to design ACE inhibitor to combat high blood pressure. In ongoing pursuit of a pharmacist career, I learned that an application of
medical knowledge such as ACE inhibitor involves much more complex issues. Before treating ACE inhibitor to patient, understanding the side effects,
drug–drug interactions, and other therapeutic interactions is critical to ensure the safety and efficacy of the medicine. In this aspect, I find the role of
pharmacist compelling in that the pharmacist is essential in informing and executing proper medication distribution to patients. Furthermore, pharmacy
incorporates both the knowledge of chemistry with health care, which I am both profoundly dedicated with. In my high school years, as a member of
Academy of Science and Medicine, I indulged myself in the environment of medical science. Developing knowledge about biotechnology such as PCR,
gel–electrophoresis, and transformation inspired me to set my heart for health care field. However, with unfortunate financial circumstances in my
family, this

Angiotensin-Converting Enzymes
In the modern medical society, scientists/doctors have adopted the use of medicines known as Angiotensin–converting enzymes or ACE inhibitors
which are ideal for treating kidney, blood vessel and heart problems (Updated by: Michael A. Chen, 2015).This particular medicine works by
lowering blood pressure and ultimately manages any disease to prevent it from getting any worse. Often patients with heart failures will be prescribed
with this medicine. This essay will give a detailed explanation and description of the benefits, side effects as well as the physiological mechanism of
ACE inhibitors.
Mechanisms of Action
How do these inhibitors work? These agents prevent an enzyme from producing angiotensin 2 (Casas et al., 2005).As a result of ... Show more content
on Helpwriting.net ...
It has also been shown that the utilisation of ACE inhibitors in patients will lower the incidence of new type 2 diabetes (Gillespie et al., 2005).
Trials with a total of over 60,000 patients have shown the ACE inhibitors reduced symptoms in the coronary artery disease as well as type 2 diabetes
however further results have shown it had no effect on patients in terms of reducing cardiovascular, cerebrovascular problems (Gillespie et al., 2005).
Conversely other research trials have shown that the use of Telmisartan inhibitors was able to moderately reduce the risk of strokes, myocardial
infarction and cardiovascular death (Effects of the angiotensin–receptor blocker Telmisartan on cardiovascular events in high–risk patients intolerant to
angiotensin–converting enzyme inhibitors: a randomised controlled trial, 2008). ACE inhibitors have also been proven to be able to help patients with
asymptomatic left ventricular systolic dysfunction (McMurray et al.,

Pathophysiology Case Study Essay
Pathophysiology case study 2
K.H. is a 67–year–old African–American man with primary hypertension and diabetes mellitus. He is currently taking an angiotensin–converting
enzyme (ACE) inhibitor and following a salt–restricted weight loss diet. He is about 30 pounds over his ideal weight. At his clinic visit his blood
pressure is noted to be 135/96. His heart rate is 70 beats/min. He has no complaints. His wife brought a blood pressure cuff and stethoscope with her in
the hope of learning to take her husband's blood pressure at home.
What risk factors for primary hypertension are evident from K.H.'s history and physical data?
Primary hypertension can be linked to several risk factors, some in which are evident in K.H.'s history and ... Show more content on Helpwriting.net ...
Physical exercise can also help the weight loss process, in turn lowering high blood pressure. Excessive smoking and drinking also leads to
hypertension due to hardening of the arteries. Family history and high stress levels should also be determined if present in KH as they play a large
role in hypertension as well (Mayo Clinic).
What is the rationale for treating K.H. with an ACE inhibitor? What is the mechanism of action?
ACE inhibitors are important and useful in the medication and treatment for KH due to their effectiveness in treating hypertension. ACE inhibitors
will help treat KH by slowing the angiotensin converting enzyme (ACE). Angiotensin II is produced by the body that can cause vasoconstriction
of the blood vessels. Angiotensin II is made from Angiotensin I by the ACE. If the production of Angiotensin II is slowed by the ACE inhibitor, the
blood vessels will be able to dilate, and blood pressure is able to be lowered (Copstead and Banasik). Thus, it is important for KH to stay on the ACE
inhibitors due to his blood pressure readings. KH's blood pressure is 135/96. His systolic blood pressure is in the pre–hypertensive range, however, his
diastolic blood pressure is in the hypertensive range and therefore, his blood pressure is hypertensive. Since his blood pressure is high, it is important
for KH to remain taking the

Hypertension Essay
Hypertension is one of the major risk factors for the development of cardiovascular diseases including stroke and may also have a role in the
development of vascular cognitive impairment and vascular dementia [1, 2]. Angiotensin I–converting enzyme (EC 3.4.15.1; ACE) plays an important
role in the rennin–angiotensin system and it is a carboxyl–terminal dipeptidyl exopeptidase that catalyzes the conversion of angiotensin I to angiotensin
II [3–6]. ACE converts an inactive form of decapeptide, angiotensin I, to a potent vasoconstrictor, octapeptide, angiotensin II, in addition; since the ACE
is a multifunctional enzyme it also catalyzes the degradation of bradykinin, which is known as a vasodilator [4, 7]. Therefore, inhibition of ACE...
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Secondary or primary metabolites produced by these organisms may be potential bioactive compounds of interest in the food and neutraceutical
industries. The worldwide demand is growing for seaweeds as useful resource for food ingredients and processed foods [22, 23]. Therefore, algae can be
a very interesting natural source of new compounds with biological activities that could be used as functional ingredients. E. cava, a kind of brown
alga (Laminariaceae) that is found abundantly in the sub tidal regions of Jeju Island, Korea and Japan [24]. It is plentifully produced Jeju Island of
Korea for commercial purposes. This brown seaweed is popular in Korea and Japan as a food ingredient, supplement of animal feed and fertilizers [25].
In addition, increasing number of scientific papers published for last few years highlighting that various biological activities and their possible
industrial applications of the brown seaweed E. cava.
Polyphenol has been emerging as one major category of natural products that is important to human health. Increasing scientific evidence shows that
polyphenols are good antioxidants, are effective in preventing cardiovascular and inflammatory diseases, and can also be used as chemo–preventing
agents for cancer [26]. Phlorotannins (brown–algal polyphenols) are the least studied group of tannins and are found only in brown algae.
Phlorotannins, a subgroup of tannins, are produced entirely by polymerization of

What Are The Negative Effects Of Chemotherapy Related...
The Negative Effects of Chemotherapy Related Diarrhoea on Systems Homeostasis
Important information for new physiologists working with CRD affected patients
Patients suffering from chemotherapy related diarrhoea (CRD) will face a multitude of social and physiological challenges, and it's important to
understand that the chronic nature of CRD is the basis for most of them. Within hours of the onset of symptoms, isotonic dehydration will rapidly lead to
hypovolemia and consequently; tachycardia, hypertension, delayed capillary refill and slightly reduced blood flow to the brain. In these early stages of
dehydration and mild hypovolemic shock – the body, while not performing optimally, is within its homeostatic limits and is not susceptible ... Show
more content on Helpwriting.net ...
The chronic increased stress on the cardiovascular system imparted by the action of these homeostatic regulators, drastically increases risk of
ischaemic heart disease later in life and forms some of the basis for the pathophysiology of other major systems. If fluid losses become too severe
and electrolytic imbalance cannot be remedied by the release of aldosterone, cerebral oedema and death can result. In less severe but chronic
dehydration, the large water content of the brain is tapped into for use in more vital physiological processes, and as a consequence the hydrolysis of
ATP that is so important for maintaining brain activity is not as efficient. Over time grey matter in the brain shrinks and the decreased efficiency adds
to the symptoms of memory impairment and lethargy. Even slightly impaired cognition and memory, headaches, lethargy and light headedness will
take a significant toll on everyday life if the patient is considering returning to work or study.
Especially in Australia where summer temperatures regularly rise above 38В°C and a significant proportion of the working population is made up of
manual labourers, it's important to note that the bodies main cooling system can shut down in very severe dehydration. This presents as inactivity of
eccrine sweat glands and in serious heat–waves the reduced fluid volume and inability to reduce core temperature causes a huge number of homeostatic
problems. Notably, as hyperthermia

Mandatory Synthesis Essay
Angiotensin II receptor blockers (ARBs) on the other hand, block angiotensin II receptor sites. ARBs have a similar mechanism of action to ACEI.
Where ACEI stops the production of angiotensin II, an ARB prevents angiotensin II from binding to the receptor cites. The outcome of this
medication would be much the same as an ACEI. On an ARB the patient would exhibit vasodilation, decreased blood volume, and decrease
ventricular remodeling. One major difference in the two classes is that ARBs have less incidence of cough because they do not inhibit Kinase II. This
would make ARBs a great second choice for patients who could not tolerate the side effects of an ACEI. Although ARBs can extend the life of a
patient in heart failure, there is no conclusive... Show more content on Helpwriting.net ...
They are considered a first line drug to treat hypertension and heart failure. Overall, diuretics will decrease blood volume, decrease venous and
arterial pressure (preload and afterload), and decrease edema both peripheral and pulmonary (Burcham 519). Thiazide diuretics are mild and only work
with relatively normal glomerular filtration rate; if the patient has low GFR a thiazide will not provide optimal benefits. When low GFR is indicated a
loop diuretic may be the better choice. These diuretics produce an exceptional amount of fluid loss; therefore, these drugs should be reserved for
patients with especially decreased cardiac output. When combined with an ACEI or and ARB, both the thiazide diuretic and the loop diuretic could
substantially improve symptomatic complication in the patient; however, the patients can experience some adverse side effects. Both can cause
hypokalemia due to the increased water elimination, this can be avoided by including a potassium supplement in the daily routine or conscientiously
eating foods high in potassium. Potassium–sparing diuretics can cause hyperkalemia because of the potassium sparing effects, especially when paired
with an ACEI or

Reaction Paper On Ramipril
TRITACE (Ramipril)
AilГse Furlong
1.0 Introduction
Tritace is an Angiotensin–Converting–Enzyme (ACE) Inhibitor. It is primarily used in the treatment of hypertension, heart failure, stroke, myocardial
infarction and diabetes. Its generic name is Ramipril. Other brand names include Altace, Cardace, Ramiril and Ramacor. Some examples of other ACE
Inhibitors are Enalapril, Quinapril, Captopril and Lisinopril. The oral bioavailability of Tritace is 55%. The absorption is not significantly affected by
food and the duration of action is 24 hours.
2.0 Physiology of Renin–Angiotensin–Aldosterone System (RAAS)
Baroreceptors located in the aortic arch and carotid sinuses detect changes in blood pressure. When a drop in blood pressure is detected, ... Show more
Depending on the patient's tolerance, the dose should be increased. It may be doubled after one or two weeks of treatment and after another two to
three weeks the dose can be increased to the target maintenance dose of 10mg of Ramipril daily.
5.2 Symptomatic Heart Failure
In patients stabilised on diuretic therapy, the recommended initial dose is 1.25 mg daily. The dose should be doubled every 1–2 weeks up to a
maximum dosage of 10 mg with two administrations daily.
5.3 Hypertension
The dose should be tailored individually to each patient based on their profile and blood pressure control. The initial recommended dose is 2.5 mg
daily. Patients with a strongly activated renin–angiotensin–aldosterone system (RAAS) may experience an excessive drop in blood pressure following
the initial dose. A starting dose of 1.25 mg Ramipril is recommended in these patients and they should be monitored closely. The dose can be doubled
every 2–4 weeks until the target blood pressure is achieved without exceeding the maximum dose allowance of 10 mg daily.
6.0 Contraindications
Hypersensitivity to ramiprilat (active metabolite)
History of angioedema
Extracorporeal treatments e.g. dialysis
Significant bilateral renal artery

Glasgow Coma Scale And The Renin-Angiotensin System
Question 1:
An unaltered consciousness occurs when the Renin–Angiotensin (RAS) system is working at 100% (Blyth & Bazarian, 2010). When changes such as
head traumas, aging, concussions, strokes, etc. occur the RAS system would be damaged overtime (Barritt & Smithard, 2011). The more often these
occur, the more it is damaged. If RAS does not seem to be working adequately it would mean that it is not be properly communicating with the cerebral
cortex, this then causing the patient to become less alert (Craig, 2003). His consciousness can only be tested by external stimuli to test for the
functioning of the RAS (through Auditory/Visual stimuli which in turn activate RAS). This is why theGlasgow Coma Scale (GCS) is used as a measure
a conscious state (Braine & Cook, 2017). It tests and scores the visual, verbal and motor response. The lower the GCS score the more of an altered
conscious state the patient is said to have. Typically the lower scores also have a worsened prognosis and/or poorer outcome on the Glasgow
Outcome Scale in an adult (Weir, et al., 2012). Mr Shepard had altered level of consciousness at a GCS of 12. When a patient has no altered level of
consciousness they are given a score of 15 (Mena, et al., 2011). Anything less than that actions need to be implemented to prevent further deterioration
and try to bring the GCS back to 15 so there is no altered conscious state. Your conscious state is affected by two main things;oxygen and glucose
(Mergenthaler,

Symptoms And Treatment Of Hypertension Essay
3.According to the B.P value, what stage of hypertension is M.K. experiencing? Explain the rationale for her current medications for her hypertension.
Also, discuss the impact of this disease on the U.S population. According to the blood pressure in the assessment, M.K. has stage one hypertension. It
was noted that she is currently being prescribed Lasix and Lotensin to help with her high blood pressure. Lotensin, also known as Benazepril, is an
ACE–inhibitor, or angiotensin–coverting enzyme inhibitor. These types of drugs play an important role in the RAAS (which stands for
renin–angiotensin–aldosterone system). Arterial blood pressure is regulated and accomplished through neural, hormonal, and renal interaction and is in
tune with the homeostatic fluid volume of one's body. The balance of sodium and water is performed by the kidneys and the
renin–angiotensin–aldosterone system is the main regulator of fluid volume in the body. An increase of extracellular fluid increases vascular
resistance, which in turn leads to increased arterial blood pressure. The kidneys will then sense this pressure change and in order to compensate, will
promote sodium and water loss through micturition. Sodium intake is directly proportional to arterial blood pressure and since the kidneys cannot get
rid of sodium as fast as water, higher levels are expected. As sodium increases serum osmolality triggering the hypothalamus to act as the regulator by
signaling the posterior pituitary gland to

Hypertension : Hypertension And Essential Hypertension Essay
Hypertension is widely considered to be one of the most important risk factors of cardiovascular diseases (angina, arrhythmia, etc.). It is the second
leading disease that causes mortality in the world. Hypertension is the condition when there is an increase in the force of blood on the walls of vessels.
It can also be defined as an arterial blood pressure that is raised above 140/90 mm Hg (systolic/ diastolic BP). Hypertension can be classified into
Secondary hypertension and Essential hypertension. When specific cause is evident but heredity, and various physiological parameters play a role in
increasing blood pressure is known as Essential Hypertension. Secondary Hypertension is one where the cause is known. According to WHO
guidelines between 2006 and 2015, deaths due to cardiovascular diseases are expected to increase by 17% while the deaths from infectious diseases,
nutritional deficiencies, maternal and prenatal conditions are projected to decline by 3%. The main causes of hypertension includes the age ,hereditary,
gender, extra weight, alcohol consumption, stress life, lazy life etc.
Basically, arterial blood pressure (BP) is directly proportional to the product of blood flow (cardiac output, CO) and the resistance to passage of blood
through pre–capillary arterioles (peripheral vascular resistance, PVR) Hypertension can be caused by either an increase in Cardiac Output (CO) or by
an increase in Peripheral Resistance (PR) BP = CO X PVR
Renin Angiotensin

Effects Of Rooibos Tea
Rooibos tea is a highly consumed hot beverage by many worldwide for its sweet flavor and great aroma. The tea is prepared from a South African
endemic plant Aspalathin linearis. The escalation of Rooibos consumption over the years paralleled the rise of consumer concerns of the importance of
food and beverages in prevention of health threats and diseases (Joubert et al., 2013). The study by Steenkamp and co–workers (2004) demonstrated
high radical scavenging ability of superoxide and hydroxyl of Rooibos extract that superseded that of other commercially available South African
herbal teas which are honey bush tea and roselle scientifically called (cyclopia intermedia)and (Hibiscus Sabdariffa L.) that are commercially available.
Rooibos tea ... Show more content on Helpwriting.net ...
It brings–about the conversion of the decapeptide Angiotensin I to the potent vasoconstrictor Angiotensin II causing increases in the blood pressure
by narrowing the blood vessels (Zhao and Xu., 2008). Blood vessels narrow because the Bradykinin which causes the blood vessels to dilate is being
degraded by the ACE in Kenin–Kallikrein System consisting of proteins that form part in inflammation (Hemming., Selkoe.,

Angiotensin Research Paper
Angiotensin– Converting Enzyme Inhibitors also known as ACE inhibitors that are commonly used to decrease blood pressure. ACE inhibitors
block the production of angiotensin I to angiotensin II which then decrease the levels of angiotensin II and elevated levels of bradykinin. ACE
drugs are also used to treat heart failure, diabetic nephropathy, and MI. The blockage of angiotensin I to angiotensin II can produce vasodilation,
decrease blood volume, decrease cardiac and vascular remodeling, potassium retention and fetal injury which are all possible side effects for ACE. A
big thing to note about ACE it that it should not be given to women who are of childbearing age due to the risk for fetal injury, especially if they are in
their second or third trimester of pregnancy. Since ACE inhibitors can increase bradykinin levels they potential side effect for that is vasodilation, ACE
cough, angioedema. If a patient presents with signs of edema in their eyes, tongue and lips this could be sign of angioedema which is life threatening
and patients should be sent to the hospital and not take ACE inhibitors anymore. ... Show more content on Helpwriting.net ...
This cough is the main reason why somebody would stop taking this medication. If patients experience a cough that is dry, nonproductive and
persistent they should stop the medication and go to the emergency room. Other adverse effects to keep in mind will be first–dose hypotension,
hyperkalemia, renal failure and neutropenia.
Like many drugs ACE inhibitors should be carefully used with patients who might be taking diuretics, antihypertensive agents, drugs that increase
potassium levels, lithium, and NSAIDS. Common ACE inhibitor drugs are Benazepril, enalaprilat, captopril, enalapril, lisinopril, ramipril, and
fosinopril. All of them are only taken orally excluding

Tenapor and Sodium Intake
The average American consumes more than double the daily recommendation of sodium. These levels are above the upper limit that is considered to
have no adverse effects on our bodies. The CDC lists heart disease as the most common cause of death for Americans, as well as kidney disease at
number nine on the top ten causes of death. These are conditions that can be exacerbated by high sodium levels. Not only that, but high blood pressure
affects nearly 1/3 of Americans and chronic kidney disease effects about 10% of the population. These are conditions in which reduced sodium in take
could be very therapeutic. Especially considering that these very common medical conditions cost many billions of dollars a year to treat. Tenapanor
has been developed to help meet the needs of those who need to reduce their sodium intake.
Tenapanor acts on the twelve transmembrane protein channel known as the sodium hydrogen exchanger 3 (NHE3) which work how the name would
suggest. By binding to this channel tenapanor blocks the sodium from being absorbed at the intestinal level which leads to it traveling straight
through the body instead of being filtered by the kidneys (Zachos et al., 2005). NHE3 channels are highly expressed on the apical regions of
enterocytes, whereas related the related sodium hydrogen exchanger 2 (NHE2) channels are more heavily expressed on the apical side (Barbry and
Hofman, 1997). This gives tenapanor a unique ability to regulate sodium levels at the point where we

Serial Blod Pressure Readings Classify Hypertension
As the blood is forced throughout our body, there is a pressure that is exerted on the walls of our arteries, this is known as blood pressure. We see
blood pressure represented as two numbers, the systolic (top) and the diastolic (bottom) numbers. The systolic blood pressure is the heart contracting
and the diastolic is the heart relaxing. A normal, healthy, blood pressure would be written as 120/80 mmHg (millimeters of mercury) or verbally
expressed by most individuals as 120 over 80. Our blood pressure can vary depending on many things. When the diastolic or systolic pressure is high,
or significantly and consistently above 120/80 mmHg, this is what we call hypertension. There are different stages or degrees of hypertension.
Lippincott Williams and Wilkins (2010) describes the stages as the following:
Serial blood pressure readings classify hypertension:
–Prehypertension: Systolic blood pressure greater than 120 mmHg but less than 90 mmHg.
–Stage 1 hypertension: Systolic blood pressure greater than 139 mmHg but less than 160 mmHg or diastolic blood pressure greater than 89 mmHg but
less than 100 mmHg.
–Stage 2 hypertension: Systolic blood pressure greater than 159 mmHg or diastolic blood pressure greater than 99 mmHg. (p. 58)
Hypertension can be identified as either primary or secondary hypertension. Primary hypertension is the most common and is typically due to factors
like age, race, level of stress, obesity, diet, tobacco use, and/or alcohol consumption in

Renal Regulation of Blood Osmolarity
Abstract: The experiment was done to demonstrate the effect of ADH on the volume and concentration of urine in order to demonstrate the control of
ADH over blood plasma osmolarity. Since non–invasive methods were preferred the volume and concentration of urine was used in place of drawing
blood. The results that we our anticipating are that ADH levels in the group of subjects that ingested the 6 gm. Of NaCl would increase over time in
response to the increased osmolarity of the blood from all of the salt. Urine output would decrease and eventually the body would stabilize.
Purpose: In this experiment, renal regulation of osmolarity will be demonstrated through the use of urinalysis.
Materials and Methods: In this experiment, ... Show more content on Helpwriting.net ...
The purpose of executing this experiment was to essentially illustrate our body's compensatory mechanisms via hormone regulation to maintain
homeostasis. Osmolarity of bodily fluids need to be in their appropriate "normal ranges" in order for the body as a whole to maintain "normal or
healthy" functions. A disruption of homeostasis will eventually lead to disease whether acute or chronic if the compensatory mechanisms within our
bodies are not working appropriately. Although the kidneys are the focus of the action, renal regulation of osmolarity goes well beyond the kidneys.
The hormones involved in the process are ADH, aldosterone, and the few involved in the renin–angiotensin system. Due to the fact that ADH was the
target of our experiment, we will begin with the anatomy and physiology involved with ADH. The cell bodies of the supra–optic nucleus of the
hypothalamus are the site of synthesis of ADH, and the site of the osmoreceptors that detect changes in blood osmolarity. The posterior pituitary is the
site of release for ADH. When the osmoreceptors detect a change in osmolarity the number and intensity of the action potentials fired will change. An
increase will cause an increase in action potentials fired from the supra–optic nucleus to the posterior pituitary via the infundibulum. Likewise, a
decrease in osmolarity will decrease the action potentials fired. The synaptic vesicles of the posterior pituitary will then secrete the appropriate

Angiotensin 2 Research Paper
The RAS is a hormone system that is responsible for maintaining homeostasis in relation to vasodilation or vasoconstriction, vascular or cardiac cell
growth and mediating oxidative stress. (Vlachogiannakos et. al. 2001) The RAS is under sympathetic nervous control and can be influenced by an
individuals weight, diet or amount of insulin. (White 2007) As illustrated by figure 1, The RAS involves the release of angiotensinogen from the
liver, which undergoes cleavage by renin to produce Angiotensin I. This is then converted to angiotensin II by ACE. Angiotensin II is a powerful
vasoconstrictor as well as being able to induce vascular and cardiac myocyte growth, and increases oxidative stress in cardiovascular and renal tissues.
All the effects of angiotensin II assist in... Show more content on Helpwriting.net ...
(White 2007) If there is an increased amount of angiotensin II circulating in the capillaries there will be net dis–inhibition of sympathetic nervous
system outflow causing an inappropriately high blood pressure. ACE inhibitors are used to counteract increased angiotensin II levels and prevent high
blood pressure or hypertension.
Mechanism of action
Under normal conditions ACE cleaves the C–terminal dipeptide from angiotensin I to form the active form octapeptide angiotensin II, ACE inhibitors
prevents this cleavage. ACE I is found in most tissues of the body with its highest concentrations being in the kidney and lungs. (Izzo & Weir 2011) As
well as inhibiting the formation of angiotensin II, ACE inhibitors prevent the degeneration of bradykinin. Bradykinin's primary role is to modulate
venous return and to assist in systemic arteriole dilation. Bradykinin is a peptide that stimulates the release of nitric oxide (NO), promoting the

The Physiological Effects of Renovascular Hypertension...
Renovascular hypertension, also known as renal hypertension, is a condition in which chronically elevated high blood pressure is caused by a
narrowing of the renal arteries. The renal arteries are the arteries that bring blood to the kidneys (9). This blood is processed by which the kidneys
filter the blood, removing some substances and sometimes adding others. The kidneys also have several functions, which can be negatively affected by
renovascular hypertension. One function is the regulation of water and ion balances within the body. In order to do so, the kidney is also responsible
for the removal of waste products and foreign chemicals from the blood by excreting them in the form of urine. Another function of the kidneys is ...
Show more content on Helpwriting.net ...
Concept 1: Renal Artery Stenosis as the Cause of Renovascular Hypertension
Renovascular hypertension is most commonly caused by prerenal factors, which are conditions that result in a decrease in blood flow to the
kidney, which is also known as hypoperfusion. In many cases, the prerenal factor that causes renovascular hypertension is renal artery stenosis.
Renal artery stenosis is defined as the narrowing of the renal artery that produces a decrease in blood flow into the kidneys (3). Renal artery
stenosis is most often caused by atherosclerosis (1). Atherosclerosis occurs when there is a buildup of fatty substances within the walls of the
arteries, which is what causes the narrowing. The fatty substances, like cholesterol and triglycerides, harden over time and become plaque, which
increases the resistance of the arteries by decreasing the circumference, but also by making the arteries less elastic (5). When arteries are less elastic,
they are unable to expand and recoil properly, which causes stiffening. Factors that can lead to atherosclerosis include a poor diet that is high in fat,
physical inactivity, and cigarette smoking (1). When the narrowing of the renal artery occurs, there is a decrease in blood flow

The Severity Of The Raas: Angiotensinogen
The functionality of the RAAS involves several different organs in the body. This process begins with a product of the liver called angiotensinogen.
Angiotensinogen is a precursor molecule that is acted upon by renin. The primary organs involved with renin production are obviously the kidneys.
Renin is created and stored in the kidneys. The renin that is produced there, as mentioned before, has a direct affect on other organs and systems as
well. Once renin has been released from the juxtaglomular cells, it acts on a substrate called angiotensin. A substrate is a molecule that is acted upon
by an enzyme. In this case, the enzyme is renin and the substrate is angiotensin. When this proteolytic change occurs, it transforms the angiotensin

What Is Angiotensin-Converting Enzyme Inhibitors?
Angiotensin–Converting Enzyme Inhibitors (ACE Inhibitors) are a group of drugs that belong to the antihypertensive drug class. There are currently
10 ACE inhibitors that are available. ACE inhibitors can be taken either by themselves or can be combined with a calcium channel blocker or a
thiazide diuretic to enhance the treatment This group of drugs is often used as a first line of treatment to treat both heart failure and hypertension. Some
of these drugs include; benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), and fosinopril (Monopril) (Lilley, p. 348). The medical
diagnosis to take ACE inhibitors includes hypertension and can be used as an adjunct for heart failure. These drugs are considered to be the drug of
choice ... Show more content on Helpwriting.net ...
All ACE inhibitors cross the placenta (Vallerand, p 164), which can cause injury or death to a fetus if taken while pregnant. Also if a patient has a
baseline potassium level of 5 mEq/L, they may be recommended not to take ACE inhibitors due to the risk of causing hyperkalemia(Lilley, p. 349).
ACE inhibitors should be used cautiously in those with any renal or hepatic impairment, hypovolemia, or hyponatremia (Vallerand, p. 165). ACE
inhibitors can cause excessive hypotension when used with diuretics or other antihypertensive drugs. Also, they should be used cautiously when taking
potassium supplements. NSAID's can potentially block the antihypertensive effects of the ACE inhibitor and should be avoided. Potential food
interactions can occur due to food dramatically decreasing the absorption of certain ACE inhibitors including captopril and meoxipril. These drugs
should be taken at least one hour before meals to ensure proper absorption (Vallerand, p. 165). Some common side effects that are associated with
taking ACE inhibitors include; nonproductive cough, hypotension, taste disturbances, diarrhea, nausea, and vomiting (Vallerand, p. 165)). Significant
effects they can have on the central nervous system include, headaches, mood and behavior changes, fatigue and dizziness. More dangerous reactions
include angioedema, hyperkalemia, and renal

Current Treatments Targeting Raas And Its Effect On The...
CURRENT TREATMENTS TARGETING RAAS
Because the RAAS has such a profound effect on the increase of blood volume during HF, it is an excellent target for many therapeutic agents. Current
pharmacological treatments for HF that target the renin–angiotensin–aldosterone system include ACE inhibitors and Angiotensin II receptor blockers
(ARBs).
ACE inhibitors such as Captopril block activity of the enzyme ACE and therefore the conversion of angiotensin I to angiotensin II (the most bio active
product of the RAAS), thus inhibiting the actions of angiotensin II and leading to decreased aldosterone production, decrease blood volume and reduced
hypertension. ACE inhibitors also work to decrease fibroblast activity as a protective measure against remodelling of the left ventricle (19). Side
effects of ACE inhibitors include a dry cough due to the inhibition of bradykinin break down, hypotension and hyperkalemia (due to higher levels of
potassium reuptake). ACE inhibitors are currently one of the drugs of choice to treat patients with HF.
ARBs such as Lostaran compete with angiotensin II to bind to the AT1 receptors and prevent the systemic effects of increased levels of angiotensin II
in HF (23). This acts to prevent the blood pressure increasing effects of the RAAS. These drugs are generally better tolerated than ACE inhibitors and
they do not inhibit bradykinin breakdown so patients do not demonstrate the dry cough associated with ACE inhibitors. Side effects of angiotensin II
receptor

Dehydration Lab Report
Hydration plays a fundamental role in body function. As such, fluid intake and excretion are tightly regulated by various heterogeneous body
mechanisms that work together to maintain a homeostatic fluid balance. Fluid and solute balance affects every organ system in the body, especially,
the cardiovascular system, the nervous system, the genitourinary system, and the various fluid compartments such as the interstitial and intracellular
spaces. Dehydration occurs when there is an extracellular fluid volume deficit and can originate from a variety of diverse causes. It can be the result of
insufficient fluid intake, excess fluid loss, or a combination of the two. Common causes of excessive fluid loss that lead to dehydration include
unmonitored... Show more content on Helpwriting.net ...
These mechanisms include activation of the sympathetic nervous system (SNS), which elicits systemic vasoconstriction (via catecholamine binding of
О±1 receptors) in an attempt to increase peripheral vascular resistance (PVR), and increases heart rate (via catecholamines binding to ОІ1 receptors) in
an attempt to increase CO, both of which are fundamental components of the blood pressure equation. This is done to maintain an adequate perfusion
pressure in order to oxygenate the tissues and prevent hypoxic cell injury. If hypovolemia is present, the body will first shunt the blood away from
less critical organs such as the GI tract in order to maintain perfusion of critical organs such as the brain, the heart system, and the kidneys. If
hypovolemia and tissue hypoperfusion are severe enough, major organ damage will occur as a result of hypoxia (Copstead & Banasik, 2013). This
patient experienced clear signs of systemic tissue hypoperfusion secondary to severe hypovolemia as evidenced by his syncopal episode (cerebral
hypoperfusion), his persistent pressure–like chest pain (myocardial ischemia), and his acute renal failure (renal hypoperfusion). The fact that these
critical organs were affected indicates just how severe his state of hypovolemia, hypotension, and hypoperfusion

Renin Angiotensin Aldosterone System Analysis
Renin Angiotensin Aldosterone System (RAAS) is the system that regulates blood pressure in the body. When the body detects low blood pressure
(low fluid/low salts), the liver releases angiotensinogen (Bayer pharma, 2015). The release of the angiotensinogen is the beginning of the signal
transduction pathway (Bayer pharma, 2015). The angiotensinogen and renin react together to form angiotensin I, then angiotensin–converting enzyme
(ACE) converts angiotensin I into angiotensin II (Bayer pharma, 2015). Angiotensin causes vasoconstriction in the blood vessels, secretes the
water–retaining hormone vasopressin (AVP) from the pituitary gland, and also releases adrenaline, noradrenaline, and aldosterone from the adrenal
gland (Bayer pharma, 2015). Overall blood pressure is most prominently regulated by the peptide angiotensin II. The angiotensin II controls
vasoconstriction through the regulation of water and salt balance (Lopez 2003). The RAAS is an essential pathway for the body to regulate blood
pressure in the body, but this pathway ... Show more content on Helpwriting.net ...
ATRAP is found in many organ systems of the body but the highest concentration of ATRAP is found in the kidneys (Giani 2013). With the advances
of gene targeting technology, the physiological role of ATRAP has been better defined (Giani 2013). For example in the experiment Angiotensin II type
1 receptor–associated protein: a novel modulator of angiotensin II actions in the nephron they eliminated ATRAP from the system it showed an
elevation in blood pressure by about 8mm/Hg in mice (Giani 2013). In the experiment Giani found that mice with ATRAP knockout had elevated
plasma and blood volume, which means the absence of ATRAP caused increased sodium and water retention by the kidneys (Giani 2013). Through the
experiment Giani concluded that ATRAP was a blood pressure modulator based on ATRAP's negative effects on proximal tubular ATR function (Giani

Hypertension And Its Effects On Hypertension
WHAT IS HYPERTENSION
ERICA SAAVEDRA
PALM BEACH VOCATIONAL INSTITUTE
WHAT IS HYPERTENSION
Hypertension, sometimes known as "Silent Killer" is America's freighting combative illness we struggle to regulate. Due too many health risk factors,
many people are sometimes unaware of hypertension until suffering from severe damaging effects.
High blood pressure is a growing problem in today's life Controlling it is the key priority.
Approximately 50 million people in the United States are affected by hypertension and approximately 1 billion worldwide. In this paper, it will outline
different topics that will help better understand, What is hypertension, Causes and Affects to Hypertension, Medication treatments that help regulate,
and Hypertension Programs that are available in helping regulate this illness.
ANATOMY, PHYSIOLOGY, AND PATHOPHYSIOLOGY OF HYPERTENTION Hypertension, as we all know the term High Blood Pressure, is
defined as a systolic pressure greater than 140 mm Hg and the diastolic pressure greater than 90 mm Hg. Hypertension is a Chronic medical condition
that occurs when blood flow in the arteries are high causing artery walls to narrow and thin, blood pressure is the result of two forces the amount of
blood measured being pumped out of the heart and into the arteries and the amount of time heart rest between each heartbeat . Systolic pressure occurs
when the left ventricle is mostly contracted, the diastolic preforms when the left

The Failure Of Heart Failure
ABSTRACT
Heart failure is one of the leading causes of mortality, both globally and in New Zealand. It is defined as the inability of the heart to meet the bodies
metabolic need for oxygen and is characterised by a decrease in cardiac output. The body has many intrinsic mechanisms to attempt to maintain cardiac
output, including activating the renin–angiotensin–aldosterone system (RAAS). The RAAS cascade acts to restore cardiac output by increasing fluid
retention, thus increasing blood volume and pressure. Unfortunately, in decompensated heart failure, this is not enough to re–establish cardiac output,
causing the action of this system to be upregulated and blood volume to increase further. This is detrimental to the already failing heart. A new drug,
aliskiren, affects the pathophysiology of hypertension and heart failure by directly inhibiting renin, a mechanism that is distinct from current therapeutic
agents that also target the RAAS, such as ACE inhibitors and Angiotensin II Receptor Blockers. This gives potential benefits by blocking the RAAS
further upstream. However, clinical trials have failed to demonstrate the predicted benefits of aliskiren. Taking this into consideration, there is a strong
possibility for development of further direct renin inhibiting agents displaying a higher potential therapeutic index for the treatment of hypertension
and heart failure. In order to thoroughly discuss the potential benefits of aliskiren in relation to hypertension and heart

The Cardiovascular System: Angiotensin
Angiotensin II is an octapeptide which is associated with the cardiovascular system. It maintains blood pressure by vasoconstriction and stimulation of
aldosterone secretion. Angiotensin II is synthesized through the renin–angiotensin system (RAS) which is known to be involved in systemic blood
pressure control, including the regulation of cerebral blood flow (Mogi, Iwanami, & Horiuchi, 2012). Renin, a product of the juxtaglomerular cells of
the kidney, is released into the circulation where it cleaves the angiotensinogen to form angiotensin I. Angiotensin I is cleaved by
angiotensin–converting enzyme (ACE) to form the angiotensin II. Apart from the production of angiotensin II in plasma and peripheral organs such as
kidney, adrenal gland, ... Show more content on Helpwriting.net ...
Both receptors are differentiated by their selective affinity for different non–peptide ligand although they have the similar binding for angiotensin II
(De Gasparo, Catt, Inagami, Wright, & Unger, 2000). Both receptors belong to the seven–transmembrane domain, G–protein coupled receptor family
(Saavedra, 2005). However, AT2 receptor shares only 32
–34% amino acid identity with the AT1 receptor. AT1 receptor was found in the areas related
to neuroendocrine control and autonomic regulation of cardiovascular function and the limbic system (Tsutsumi & Saavedra, 1991). The
physiological actions of angiotensin II in the brain, such as regulation of blood pressure, fluid balance, and hormone secretion, are mediated by the
AT1 receptor. Additionally, systemic angiotensin II affects the brain functions through AT1 receptors located in the circumventricular organs which
are devoid of BBB and derived angiotensin II may act at many sites in the central nervous system located behind the BBB (Unger & Scholkens,
2004). On the other hand, AT2 receptor acts a role in brain organogenesis and in the function of sensory and motor systems (Tsutsumi & Saavedra,
1991). However, the physiological functions of the AT2 receptor are still uncertain (De Gasparo & Siragy, 1999; Saavedra, 2005). Thus, the role of
brain angiotensin II appears to be multiple and complex

Hypertension : High Blood Pressure
HYPERTENSION
Summer 2015
Bhavneet K. Singh
High blood pressure
Definition: The heart is supplies the organs and tissues of the body with blood and nutrients it carries. It pumps blood into the blood vessels of the
circulatory system. The blood that is pumped into these vessels puts pressure on the walls of the vessels. When the heart muscle contracts during
each beat, the pressure rises as well. Blood pressure may be different at different times of the day. It is usually higher when someone first wakes up,
after exercise, or when under stress. Having higher blood pressure for short amounts of time is normal, but when blood pressure stays high for most of
the time, it can cause serious health problems. High blood pressure, also called hypertension, is a serious medical condition. It is defined as a
chronically increased systemic arterial pressure. It happens when the force of the blood pumping through the arteries is too strong. About 7 million
people die each year in the United States from illnesses caused by high blood pressure.
Blood pressure is measured in units of "millimeters of mercury" written mm Hg. When measuring blood pressure, there are two different values.
Systolic blood pressure is taken while the heart muscle is contracting and pumping oxygen–rich blood into the blood vessels. Diastolic blood pressure is
taken while the muscle is relaxing and refilling with blood. Blood pressure measurements are given in pairs, with the upper (systolic) value first

Heart Failure And Acute Kidney Injury
Our current study demonstrates that among hospitalized HF patients, 2179 (32%) had traditional AKI (rise in serum creatinine by >=0.3 mg/dl) and
789 (12%) of hospitalized HF patients developed reverse AKI (drop in serum creatinine by >=0.3 mg/dl). The change in serum creatinine of greater
than or equal to 0.3mg/dl was associated with higher 30–day all–cause readmission and mortality. Interestingly, reverse AKI group was also associated
with higher 30–day all–cause readmission and mortality. To our knowledge this is the first study that reports 30–day all cause readmission and
mortality by serial changes in serum creatinine in hospitalized HF patients. There is a need for increased awareness regarding this particular subset of
patients.... Show more content on Helpwriting.net ...
The explanation for presentation of this group is multifactorial including advanced stage of heart failure, old age, hypertension, diabetes mellitus, acute
coronary syndrome, secondary to aggressive diuresis as supported by increased use of loop and potassium sparing diuretics and an intrinsic imbalance
between the vasoconstrictive (epinephrine, angiotensin, endothelin) and vasodilatory hormones (natriuretic peptides, nitric oxide). 7
The risk of readmission and mortality in reverse AKI group is similar to traditional AKI as shown in our study. Hence the increase in creatinine is not
only a marker of severity of heart failure but also represents a pathway for accelerated cardiovascular injury.
In a study of chronic heart failure patients in ambulatory setting the authors found that worsening renal function within 6 months of referral was
prognostically associated with all–cause mortality and heart failure readmission. 8 Major studies to date predicting heart failure morbidity and mortality
do not include AKI as one of the prognostic indicators.9, 10 A recently published meta–analysis suggests that the benefit of renin–angiotensin
aldosterone inhibitor is not diminished by worsening renal function and is in fact greater in the group with the worsening renal function.11 Hence
contrary to the practice of stopping ACE/ARB in patients with AKI they are more essential in this high risk group with increased readmission and
mortality. Also

The Importance Of Evidence Based Assessment
Review the care given and provide an evidence based critique of that care It is vitally important to initiate accurate documentation and assessment
when performing a patients' observation as this can clearly prevent and identify acute poor health (Mulryan, 2011). On the other hand, an
observation assessment can to often be performed accurately and incorrectly (Mulryan, 2011). For that reason, a nurse's ability, knowledge,
competence and documentation are all paramount when assessing a patient stability (Mulryan, 2011). On evaluating the care that was given to
Sam, when being assessed every four hours for vital signs, by nurses involved in her care. Firstly, Sam was on medication for pain relief which
was helping keep her pain free. As she stated when asked in the PSA if she was in pain, Sam stated that she was not in any pain at the time.
Evidence based practice recommends that a nurse should give the patient regular analgesic and PRN analgesic when needed (Park et al, 2016).
Inadequately managed pain can lead to adverse physical and psychological patient outcomes for individual patients and their families (Park et al,
2016). inadequate pain management negatively affect the patient's welfare and the hospital performance because of extended lengths of stay and
readmissions, both of which increase the cost of care (Park et al, 2016). Secondly, due to Sam's condition she was at risk of having a high fever I
identified through the PSA Sam's temperature at the time was

An Outline Of An Assignment
Part 1
Patient
Mr Timothy Jones
38 years old
Presenting Complaint
Essential Hypertension. Blood pressure control lost on current therapy
Type of Prescribing
This is an episode of Supplementary Prescribing. It is defined as,
'A voluntary partnership between a doctor or dentist and a supplementary prescriber to implement an agreed patient specific clinical management plan
(CMP) with the patients' agreement'. (DOH, 2007) Mr Jones benefits from Supplementary Prescribing as it ensures timely access for review of his
condition along with treatment modification and subsequent monitoring with the reassurance that a GP retains the overview of his care.
The Consultation Model
I applied Neighbours Model, The Inner Consultation (Neighbour, R, 1987). This identifies a pathway which hones consultation skills by goal setting,
skill building and finally pulling everything together. The model contains five intuitive stages. See Appendix 1. The use of a model helps me to ensure
consistent and effective consultations with reproducibility which optimises outcomes for Mr Jones. They are useful as a framework from which
clinicians develop their own style (Moulton & Neighbour, 2007)
Connecting
History of Presenting Complaint
Mr Jones requires regular review and management of his Essential Hypertension which was first diagnosed 5 years ago. He has been well maintained
on lower than recommendation (NICE, 2011) dose of angiotensin converting enzyme inhibitor Lisinopril dihydrate. He has no

Question 1 . 1.1)What Steps Would You Suggest Should Be
Question 1
1.1)What Steps Would You Suggest Should Be Taken To Minimize The Loss Of Vitamins From Food?
The steps that should be taken to minimize the loss of vitamins from food is as follows
–We should do shopping for foods such as vegetables and fruit from the farm markets or supermarkets that get the fruits and vegetables directly from
the farmers. The longer the food stays on the shelves the more it losses the nutrient content therefore obtaining such foods as soon as possible after
harvesting ensures that you get nutrient rich foods before it loses its nutrient contents. Alternatively one can make a vegetable garden and plant fruit
trees such as peach trees at home, by doing this you can obtain not only nutrient rich foods by ... Show more content on Helpwriting.net ...
–It is cheaper to buy and is easily produced at low cost.
–It is easy to prepare.
–It provides consumers with a recommended daily intake.
–It is regulated by the food and drug administration council.
1.3)Explain How Cooking And Processing Methods May Increase The Bioavailability Of Beta Carotene?
–Significantly more beta–carotene is absorbed from cooked and processed foods. This is because beta–carotene is set free from the cellular matrices by
the heat from processing and cooking. This allows beta–carotene to be readily available for absorption in our body, rather than in raw vegetables where
it should first be extracted from the cellular matrices
Question 2
2.1)Fortification Programs Of Asian Versus African Countries Asian countriesAfrican countries
Staple food.SaltWheat
Micronutrient likely to be deficient in the diet.IodineIron
Name of the deficiency disease.–Hyperthyroidism
–Endemic Goiter
–Cretinism –Iron deficiency anemia
Symptoms of the deficiency disease.–Enlarged thyroid gland

–Difficulty swallowing
–Hoarse voice
–Coughing –Pale skin
–Fatigue
–Shortness of breath
–Dizziness
2.2)Name And Discuss The Method That Is Recommended By The South African Red Cross Association For The Treatment Of Rehydration Caused
By Diarrhea?
The recommended method by the south African red cross association for rehydration caused by diarrhea is called the Salt, Sugar Solution and is
abbreviated

The Silent Killer : Hypertension
The Silent Killer: Hypertension
Bernice, is an 80 year old, African American, female, who presents to the inpatient unit for further therapy after undergoing a colostomy reversal. Her
history is significant for type 2 diabetes mellitus, stage 3 chronic kidney disease, and hypertension, for which she is taking a calcium channel blocker
and a beta blocker. Her family history indicates that both her sisters and brother, had diabetes, as well ashypertension. Another key element is that
Bernice is a former smoker. Physical examination reveals a healthy weight women, with a blood pressure of 153/71 mmHg and a heart rate of 64
bpm. Lungs are clear, and cardiac examination reveals a regular rate and rhythm. Abdomen is without bruits and peripheral pulses are equal.
Laboratory results are significant for a non fasting glucose of 182 mg/dL. The patient's blood urea nitrogen and serum creatinine are 26 mg/dL and
1.82 mg/dL.
Pathophysiology of Hypertension
After the analysis of this case study, I have chosen to perform research on the patient's diagnoses of hypertension. Hypertension, also known as, high
blood pressure, is a global problem. The desired blood pressure, according to the Joint National Committee are, below 150/90 mmHg for individuals
60 years and older, and below 140/90 mmHg for individuals under 60 years of age (Beeman, 2013, p. 334). Thus, individuals not meeting this criteria
have to be treated with drug therapy. Understanding the mechanisms in which normal blood pressure is maintained, will aid in the understanding of
hypertension. Systemic arterial pressure is a product of cardiac output and total peripheral vascular resistance. To maintain a balance between these
factors, there are four control systems that play a role: the arterial baroreceptor system, regulation of body fluid volume, the renin angiotensin
aldosterone system, and vascular autoregulation (Beeman, 2013, p. 337).
Arterial baroreceptors are responsible for monitoring the levels of arterial pressure. When these baroreceptors sense a rise in arterial pressure, they
counteract by slowing down the cardiac system and vasodilating (Beeman, 2013, p. 338). Changes in body fluid volume also affect arterial pressure; a
rise in pressure occurs

The Renin-Angiotensin System
Arteries transport oxygenated blood away from the heart at a high pressure known as systolic blood pressure. Arteries will constrict and dilate
affecting the systolic blood pressure. Constriction of the arteries will increase the pressure, also known as hypertension. Dilation of the arteries will,
inversely, decrease the blood pressure, also known as hypotension. (Elsevier, 2014)
When a patient's heart is not preforming properly or a disease if affecting the blood volume, the heart will increase or decrease it's contractility overall
changing the systolic blood pressure. With congestive heart failure, the act of sodium, chloride, and water retention is detected. This is in result of the
Renin–Angiotensin System. When there is a decrease in

Case Study (Heart Failure)

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