Reaction Paper On Ramipril

Reaction Paper On Ramipril
TRITACE (Ramipril)
Ailíse 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 content on Helpwriting.net ...
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
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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 ... Show more content on Helpwriting.net ...
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

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.,

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 content on Helpwriting.net ...
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 α1–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

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 38°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

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

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

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

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

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

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

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 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

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 as hypertension. 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

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

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

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

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

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

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

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.,

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

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

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

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

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

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

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 α1 receptors) in an attempt to increase
peripheral vascular resistance (PVR), and increases heart rate (via catecholamines binding to β1
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

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 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

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

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

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 countries African countries
Staple food. Salt Wheat
Micronutrient likely to be deficient in the diet. Iodine Iron
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

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 content on Helpwriting.net ...
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

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

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 the Glasgow 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,

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 in blood.
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

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

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