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Weldone ma Odugbose Rhoda 300level nursing

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Thank you for the lecture on Anticoagulants ma. Adegbuyi Praise Toluwanimi 300 level Matric number 2023001586

Okoro Salvation Chikaodili 2023002341 300level Nursing

Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system that regulates blood pressure, fluid, and electrolyte balance in the body. Here’s a summary: 1. Activation: RAAS is activated when there’s a drop in blood pressure, blood volume, or sodium levels. The kidneys release an enzyme called renin. 2. Angiotensin Formation: Renin converts angiotensinogen (produced by the liver) into angiotensin I, which is then converted into angiotensin II by the enzyme ACE (angiotensin-converting enzyme). 3. Actions of Angiotensin II: • Vasoconstriction: Narrows blood vessels, increasing blood pressure. • Aldosterone Release: Stimulates the adrenal glands to release aldosterone, which promotes sodium and water reabsorption in the kidneys, raising blood volume and pressure. 4. Feedback Regulation: When blood pressure and volume normalize, the RAAS system reduces its activity to maintain balance. This system is crucial for maintaining cardiovascular stability but can contribute to conditions like hypertension if overactive. Adegbuyi Praise Toluwanimi 300l Nursing Matric number 2023001586

RAAS Renin Angiotensin Aldosterone System is a hormone system that plays a vital role in regulating blood pressure,fluid and electrolyte balance in the body. Component of RAAS includes the following 1.Renin: An enzyme that release by kidneys in response to decrease in blood pressure 2.Angiotensinogen:A protein produced by liver and converted to angiotensin I. 3.Angiotensin Converting Enzyme:This is an enzyme that convert angiotensin I to angiotensin II. 4.Angiotensin II:A potent vasoconstrictor that increase blood pressure thereby stimulates release of Aldosterone 5.Aldosterone:is a hormone produced by adrenal gland that promotes sodium retention and potassium excretion. FUNCTIONS: 1.Blood Pressure regulation:RAAS helps to maintain blood pressure 2.Fluid balance:RAAS regulates fluid balance by controlling sodium water reabsorption. 3.Electrolytes homeostasis:RAAS helps to maintain potassium and sodium balance. RAAS Inhibitors 1.ACE Inhibitors:This blocks the conversion of angiotensin I to angiotensin II. 2.Angiotensin receptor blockers:Itblocks the action of angiotensin II. 3.Direct Renin Inhibitors:It blocks the action of renin. 4.Aldosterone antagonist:It blocks the action of Aldosterone. 2023000854 Ikumogunniyi - Lawal Shakirat Bukola

Thanks for the wonderful lectures ma… Answer: 1) Ecchymosis on the flank of a patient is also known as Grey Turners sign. 2) Cullen's sign is seen like a bluish discolouration around the umbilical which shows that a particular organ is damaged causing bleeding. 3) Glucose increased Calcium decreased Amylase increased Lipase increased.

What a wonderful lecture, succinct and apt.

Pancreatitis is an inflammation of the pancreas. 1- Ecchymosis on the right flank on a patient is also called Turner's sign 2-Yellowish discoloration around the umbilical region is called Cullen's sign 3-glucose will increase 4-calcium wil decrease 5-amylase will increases 5-lipase increases

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The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system that plays a critical role in regulating blood pressure, fluid balance, and electrolyte levels in the body. How does it works: 1. Activation Trigger RAAS is activated in response to: -Low blood pressure (e.g., dehydration, blood loss). -Low sodium levels in the blood. -Sympathetic nervous system stimulation (fight-or-flight response). 2. Renin Release When the kidneys detect low blood pressure or low sodium: -The juxtaglomerular cells in the kidneys release renin, which is an enzyme. 3. Angiotensinogen Conversion Renin converts angiotensinogen (a protein produced by the liver) into angiotensin I. 4. Angiotensin I to Angiotensin II Angiotensin I is converted to angiotensin II by the enzyme angiotensin-converting enzyme (ACE), primarily in the lungs. 5. Actions of Angiotensin II -Angiotensin II is a powerful hormone that: -Raises blood pressure by causing blood vessels to constrict (vasoconstriction). -Stimulates the release of aldosterone from the adrenal glands. -Stimulates the release of antidiuretic hormone (ADH) from the brain to promote water reabsorption. -Increases thirst to encourage fluid intake. 6. Aldosterone’s Role Aldosterone acts on the kidneys to: -Retain sodium; water follows sodium thereby increasing blood volume. -Excrete potassium. 7. Result -Blood pressure and fluid balance are restored, resolving the initial triggers. Clinical Relevance Dysregulation of the RAAS can contribute to: -Hypertension (high blood pressure). -Heart failure. -Kidney disease. Note: Medications like ACE inhibitors, angiotensin receptor blockers (ARBs), and aldosterone antagonists target RAAS to treat these conditions. Matric num: 2023001103 300L Nursing Department.

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RAS Renin Angiotensin Converting System. Is a physiological pathway that regulate blood pressure, fluid balance and electrolyte homeostasis. Key Components 1 Renin 2 Angiotensinogen 3 Angiotensin Converting Enzymes 4Angiotensin ll 5 Aldosterone. Mechanism. Vasoconstriction Fluid retention Electrolyte balance Blood pressure regulation. Pathological Activation. Hypertension Heart failure Kidney disease. Therapeutic Targerting Direct Renin inhibitors Angiotension receptors blockers Aldosterone antagonist. Matric No 2022001293 Name Dawodu kudirat Adeyemi Level 300 Dept ..Nursing

Ebe Rhoda Abosede 2023000616 300L

The Renin-Angiotensin-Aldosterone System (RAAS) is a hormonal cascade critical for maintaining blood pressure, fluid, and electrolyte balance, as well as systemic vascular resistance. This system is activated in response to various physiological triggers, including low blood pressure, decreased sodium levels, or increased sympathetic nervous system activity. It’s key components are: 1. Renin Release: The kidneys release renin in response to low blood pressure, low sodium, or sympathetic activation. 2. Angiotensin II Formation: Renin converts angiotensinogen (from the liver) to angiotensin I, which ACE (in the lungs) converts to angiotensin II. 3. Effects of Angiotensin II: • Vasoconstriction: Raises blood pressure. • Aldosterone Release: Stimulates the adrenal glands to retain sodium and water in the kidneys. • ADH Release: Promotes water reabsorption. 4. Aldosterone: Increases sodium/water retention and potassium excretion.

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Thk you ma for the lecture. Oladele Abidemi Matric No-2023001682 300L

Thk you ma for the lecture. Oladele Abidemi Matric No-2023001682 300L

Thk you ma for the lecture. Oladele Abidemi Matric No-2023001682 300L

Abimbola Oreofe Victoria 20002406 Nursing 300L

Thk you ma for the lecture. Oladele Abidemi Matric No-2023001682 300L

Thk you ma for the lecture. Oladele Abidemi Matric No-2023001682 300L

Renin angiotensin aldosterone system (RAAS) is a series of reactions that regulate blood pressure, blood volume, and electrolyte balance. The RAAS is made up of hormones, proteins, and enzymes. Mechanism of action When blood pressure drops, the kidneys release renin into the bloodstream. Renin splits angiotensinogen into angiotensin I. Angiotensin-converting enzyme (ACE) splits angiotensin I into angiotensin II. Angiotensin II causes blood vessels to constrict, which increases blood pressure. Angiotensin II also causes the release of aldosterone, which makes the kidneys retain sodium and excrete potassium. What it regulates Blood pressure: The RAAS regulates blood pressure by increasing the reabsorption of sodium and water, and by constricting blood vessels. Blood volume: The RAAS regulates blood volume. Electrolyte balance: The RAAS regulates electrolyte balance. Vascular resistance: The RAAS regulates vascular resistance. Other effects The RAAS can also cause uremic toxin retention. The RAAS can be affected by circadian rhythms, which can cause variations in blood pressure, urine flow, and electrolyte excretion. Odenike Hibatullah Abiola 2023001343

Renin Angiotensin Aldosterone System (RAAS) is a series of reactions that regulates blood pressure, electrolyte balance and blood volume. The RAAS is activated when blood pressure drops, and involves the kidneys, lungs and adrenal glands. *STEPS:* 1. Renin releases when blood pressure drops, the kidneys release Renin into the bloodstream. 2. Angiotensinogen cleavage Renin splits angiotensinogen, a protein made by the liver, into Angiotensin I. 3. Angiotensin I conversion increase by constricting small arteries. 4. It also triggers the release of Aldosterone and vasopressin. 5. Sodium and water retention Aldosterone and vasopressin cause the kidneys to retain sodium and water, which increase blood pressure and blood volume. *EFFECTS:* Hypertension: Abnormal activation of the RAAS can lead to chronic hypertension. *Cardiac failure:* Abnormal activation of the RAAS can lead to cardiac failure. *Kidney Conditions:* Abnormal activation of the RAAS can lead to kidney Conditions. Kidney to retain sodium and water, which increases blood pressure and blood volume. *TREATMENT* : Drugs that inhibit the RAAS pathway, such as ACE inhibitors and ARBSs, can treat hypertension and cardiac failure. Name: Layeni Taofikat Bodunrin Matric Number:2023000378 Level: 300l

The renin-angiotensin-aldosterone system (RAAS) is a hormone system that controls blood pressure, fluid balance, and electrolyte levels. It also regulates the resistance of blood vessels throughout the body. How it works The kidneys release renin in response to changes in blood pressure, volume, and sodium and potassium levels. Renin converts angiotensinogen into angiotensin I. Angiotensin I is then converted to angiotensin II. Angiotensin II stimulates the adrenal glands to release aldosterone. What it does The RAAS increases sodium and water reabsorption, which raises blood pressure. It also increases vascular tone, which is the degree to which blood vessels constrict. The RAAS controls the growth of tissue in the kidneys. When it can be overactive An overactive RAAS can contribute to kidney disease, hypertension, and heart disease. Angiotensin II can cause inflammation, cell growth, and fibrosis in the kidneys. Angiotensin II can also cause cardiac hypertrophy, arrhythmia, and heart failure. How it can be treated Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) can help treat hypertension and heart failure. Aldosterone antagonists can also help treat hypertension and chronic kidney disease. 2023002084 Adebisi kuburat Tope

Thank you so much ma for the explanation. RAAS The renin-angiotensin-aldosterone system (RAAS) is the system of hormones, proteins, enzymes and reactions that regulate your blood pressure and blood volume on a long-term basis. Key component of RAAS 1. Renin 2. Angiotensionogen 3. Angiotensin 1 4. Angiotensin-converting Enzyme (ACE) 5. Antidiuretic Hormone (ADH) Akande Etana Mercy 2023002075 Nursing department 300 level

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Excellent ma Akande Etana Mercy 2023002075 Nursing department 300 level

Thank you ma ALFA FATIMA 2023000676 Nursing dept. 300l

The RAAS is a complex multi-organ endocrine (hormone) system involved in the regulation of blood pressure by balancing fluid and electrolyte levels, as well as regulating vascular resistance & tone. RAAS regulates sodium and water absorption in the kidney thus directly having an impact on systemic blood pressure. Typically, RAAS is activated when there is a drop in blood pressure (reduced blood volume) to increase water and electrolyte reabsorption in the kidney; which compensates for the drop in blood volume, thus increasing blood pressure

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Thank you for the lecture ma 2023000267 300l Nursing department

Awolola Bolanle Christianah 2023000376 300l Nursing science

The Renin-Angiotensin-Aldosterone System (RAAS) is a vital physiological pathway that regulates blood pressure, fluid balance, and electrolyte homeostasis. Components of RAAS 1. *Renin*: An enzyme released by the kidneys in response to decreased blood volume or pressure. 2. *Angiotensinogen*: A protein produced by the liver that is converted to angiotensin I by renin. 3. *Angiotensin-Converting Enzyme (ACE)*: An enzyme that converts angiotensin I to angiotensin II. 4. *Angiotensin II*: A potent vasoconstrictor that increases blood pressure and stimulates the release of aldosterone. 5. *Aldosterone*: A hormone produced by the adrenal glands that promotes sodium retention and potassium excretion. RAAS Pathway 1. Renin release 2. Angiotensinogen conversion to angiotensin I 3. Angiotensin I conversion to angiotensin II 4. Angiotensin II stimulates vasoconstriction and aldosterone release 5. Aldosterone promotes sodium retention and potassium excretion Functions of RAAS 1. *Blood pressure regulation*: RAAS helps maintain blood pressure homeostasis. 2. *Fluid balance*: RAAS regulates fluid balance by controlling sodium and water reabsorption. 3. *Electrolyte homeostasis*: RAAS helps maintain potassium and sodium balance. Dysregulation of RAAS 1. *Hypertension*: Overactivation of RAAS can lead to high blood pressure. 2. *Heart failure*: RAAS dysregulation can contribute to heart failure. 3. *Kidney disease*: RAAS overactivation can lead to kidney damage. RAAS Inhibitors 1. *ACE inhibitors*: Block the conversion of angiotensin I to angiotensin II. 2. *Angiotensin receptor blockers (ARBs)*: Block the action of angiotensin II. 3. *Direct renin inhibitors*: Block the action of renin. 4. *Aldosterone antagonists*: Block the action of aldosterone. RAAS inhibitors are commonly used to treat conditions such as hypertension, heart failure, and kidney disease.

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Much thanks for the lectures ma! Okoye Favour 2023001837 Nursing Department 300L

RAAS-THAT'S; Angiotensin Aldosterone system is important physiological pathway which help to regulate blood pressure, fluid balance and also maintains electrolyte homeostasis. The RAAS is being regulated by many mechanism which includes feedback inhibition, high blood pressure and sodium levels inhibitors renin release and reducing RAAS activity.

Wahaab Aisha Bolanle 2023000921 Nursing 300level Renin-Angiotensin-Aldosterone System (RAAS) The Renin-Angiotensin-Aldosterone System (RAAS) is a hormonal cascade critical for maintaining blood pressure, fluid, and electrolyte balance, as well as systemic vascular resistance. This system is activated in response to various physiological triggers, including low blood pressure, decreased sodium levels, or increased sympathetic nervous system activity. Key Components of the RAAS 1. Renin Origin: Secreted by juxtaglomerular cells in the kidneys. Stimuli for Release: Reduced renal perfusion pressure (e.g., hypotension). Decreased sodium concentration in the distal tubule, sensed by the macula densa. Sympathetic nervous system activation via β1-adrenergic receptors. Function: Converts angiotensinogen (produced by the liver) into angiotensin I. 2. Angiotensinogen Origin: Synthesized and released by the liver. Role: Acts as the substrate for renin to produce angiotensin I. 3. Angiotensin I Origin: Formed by the action of renin on angiotensinogen. Activity: Biologically inactive precursor. 4. Angiotensin-Converting Enzyme (ACE) Location: Primarily in the lungs, but also in endothelial cells throughout the body. Function: Converts angiotensin I into the active form, angiotensin II. 5. Angiotensin II Functions: Vasoconstriction: Increases systemic vascular resistance and blood pressure. Stimulation of Aldosterone Secretion: Promotes sodium and water retention. Stimulates ADH Release: Increases water reabsorption in the kidneys. Promotes Thirst: Enhances fluid intake to restore blood volume. Cardiac and Vascular Remodeling: Contributes to hypertrophy and fibrosis in chronic conditions. 6. Aldosterone Origin: Secreted by the adrenal cortex (zona glomerulosa). Function: Increases sodium reabsorption and potassium excretion in the distal tubules and collecting ducts. Enhances water retention, increasing blood volume and pressure. 7. Antidiuretic Hormone (ADH) Stimulated by Angiotensin II: Increases water reabsorption in the kidneys via aquaporin-2 channels in the collecting ducts. Regulation of the RAAS 1. Negative Feedback Mechanism Elevated blood pressure and volume reduce renin secretion. High sodium levels inhibit macula densa stimulation of renin release. 2. Pathological Activation Chronic activation of RAAS is implicated in hypertension, heart failure, chronic kidney disease, and other cardiovascular disorders. Clinical Implications 1. RAAS Inhibitors: Used to manage hypertension, heart failure, and kidney disease. These include: ACE Inhibitors (e.g., enalapril, lisinopril): Prevent angiotensin I to angiotensin II conversion. Angiotensin II Receptor Blockers (ARBs) (e.g., losartan, valsartan): Block angiotensin II receptors. Aldosterone Antagonists (e.g., spironolactone, eplerenone): Reduce aldosterone-mediated effects. 2. Hyperaldosteronism: Causes hypertension and hypokalemia due to excessive aldosterone production. 3. RAAS and Chronic Disease: Persistent activation leads to fibrosis, endothelial dysfunction, and organ damage.

Understood Thanks for the lecture ma Ogunwale Abidat Odunayo 2023000146 300L Nursing

What a wonderful lecture!!!. ADESINA CLARA ADEBOLA. 2023000838

When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to a decapeptide called angiotensin I, which has no biological function on its own.[4] Angiotensin I is subsequently converted to the active angiotensin II (an octapeptide) by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs.[5] Angiotensin II has a short life of about 1 to 2 minutes. Then, it is rapidly degraded into a heptapeptide called angiotensin III by angiotensinases which are present in red blood cells and vascular beds in many tissues. Angiotensin III increases blood pressure and stimulates aldosterone secretion from the adrenal cortex; it has 100% adrenocortical stimulating activity and 40% vasopressor activity of angiotensin II. Angiotensin IV also has adrenocortical and vasopressor activities. Angiotensin II is a potent vasoconstrictive peptide that causes blood vessels to narrow, resulting in increased blood pressure.[6] Angiotensin II also stimulates the secretion of the hormone aldosterone[6] from the adrenal cortex. Aldosterone causes the renal tubules to increase the reabsorption of sodium which in consequence causes the reabsorption of water into the blood, while at the same time causing the excretion of potassium (to maintain electrolyte balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure. If the RAS is abnormally active, blood pressure will be too high. There are several types of drugs which includes ACE inhibitors, angiotensin II receptor blockers (ARBs), and renin inhibitors that interrupt different steps in this system to improve blood pressure. These drugs are one of the primary ways to control high blood pressure, heart failure, kidney failure, and harmful effects of diabetes Israel Oluwatoyin Blessing 2023000342 Nursing Dept 300L

(RAAS) steps? The renin-angiotensin-aldosterone system (RAAS) involves several steps, including: When the blood pressure falls, the kidneys release the enzyme renin into the bloodstream. Renin splits angiotensinogen, a protein the liver makes and releases, into pieces. One piece is the hormone angiotensin I. Angiotensin I, which is inactive (doesn’t cause any effects), flows through the bloodstream and is split into pieces by angiotensin-converting enzyme (ACE) in the lungs and kidneys. One of those pieces is angiotensin II, an active hormone. Angiotensin II causes the muscular walls of small arteries (arterioles) to constrict (narrow), which increases blood pressure. Angiotensin II also triggers the adrenal glands to release aldosterone and the pituitary gland to release antidiuretic hormone (ADH, or vasopressin). Together, aldosterone and ADH cause the kidneys to retain sodium. Aldosterone also causes the kidneys to release (excrete) potassium through your urine. The increase in sodium in the bloodstream causes water retention. This increases blood volume and blood pressure, thus completing the raas.

IZUAGBE AUGUSTINA 2023001992 300L Nursing Science thanks for the lecture ma

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