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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

Well do ma 4:16pm

RAAS- when the blood volume drops or blood flow to the kidney reduce, kidney produces an enzyme called RENIN to the blood stream which help to convert plasma protein to angiotensionogen to angiotensin 1 and ACE convert angiotensin 1 to angiotensin 11 which is a potent vasoconstriction there by increasing the blood pressure.

Weldone ma, nice lecture, Chado maimunat Muhammad 2023000591

Thank you so much ma

Thank you ma, the lecture is understandable

Weldon ma

SADA SHEYE AYIBAINASUOTONTE 2023001042 NURSING 300L 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. --- Summary The RAAS is essential for maintaining cardiovascular homeostasis but can become maladaptive in chronic diseases. Understanding its mechanisms allows for targeted therapeutic interventions to manage a range of conditions related to blood pressure and fluid imbalances.

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The Renin-Angiotensin-Aldosterone System (RAAS) is a vital physiological pathway that regulates blood pressure, fluid balance, and electrolyte homeostasis. Here's a breakdown of the system: Components of RAAS 1. *Renin*: An enzyme released by the kidneys in response to decreased blood volume or low blood pressure. 2. *Angiotensinogen*: A protein produced by the liver that serves as the substrate for renin. 3. *Angiotensin-converting enzyme (ACE)*: An enzyme primarily found in the lungs 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 regulates electrolyte balance and fluid retention. Mechanism of Action The RAAS pathway is activated when the kidneys detect decreased blood volume or low blood pressure. Here's a step-by-step explanation: 1. Renin release: The kidneys release renin, which converts angiotensinogen to angiotensin I. 2. ACE conversion: Angiotensin I is converted to angiotensin II by ACE in the lungs. 3. Angiotensin II effects: Angiotensin II increases blood pressure by constricting blood vessels and stimulating the release of aldosterone. 4. Aldosterone effects: Aldosterone promotes sodium retention, water reabsorption, and potassium excretion in the kidneys, leading to increased blood volume and pressure. 2023000711 Nursing 300L

The Renin-Angiotensin-Aldosterone System (RAAS) is a vital physiological pathway that regulates blood pressure, fluid balance, and electrolyte homeostasis. Here's a breakdown of the system: Components of RAAS 1. *Renin*: An enzyme released by the kidneys in response to decreased blood volume or low blood pressure. 2. *Angiotensinogen*: A protein produced by the liver that serves as the substrate for renin. 3. *Angiotensin-converting enzyme (ACE)*: An enzyme primarily found in the lungs 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 regulates electrolyte balance and fluid retention. Mechanism of Action The RAAS pathway is activated when the kidneys detect decreased blood volume or low blood pressure. Here's a step-by-step explanation: 1. Renin release: The kidneys release renin, which converts angiotensinogen to angiotensin I. 2. ACE conversion: Angiotensin I is converted to angiotensin II by ACE in the lungs. 3. Angiotensin II effects: Angiotensin II increases blood pressure by constricting blood vessels and stimulating the release of aldosterone. 4. Aldosterone effects: Aldosterone promotes sodium retention, water reabsorption, and potassium excretion in the kidneys, leading to increased blood volume and pressure. Clinical Significance Dysregulation of the RAAS has been implicated in various cardiovascular and renal disorders, including: - Hypertension - Heart failure - Kidney disease - Diabetes Inhibition of the RAAS using medications like ACE inhibitors, angiotensin receptor blockers (ARBs), and direct renin inhibitors can help manage these conditions. 2023000711 Nursing 300L

Weldon ma

Please ma, we are interested in the EKG lecture ma Thank you and well done ma

RAAS (Renin-Angiotensin-Aldosterone System) is a physiological pathway that regulates blood pressure, fluid balance, and electrolyte balance. It's a complex process involving hormones and enzymes that control: - Blood vessel constriction and dilation - Sodium and water reabsorption in the kidneys - Electrolyte balance Dysregulation of RAAS is linked to conditions like hypertension, heart failure, and kidney disease. Adewuyi Temitope Glory 2023000452

RAAS stands for Renin-Angiotensin-Aldosterone System. It's a vital physiological pathway that regulates blood pressure, fluid balance, and electrolyte homeostasis. Key Components of RAAS: 1. Renin: An enzyme released by the kidneys in response to decreased blood pressure or volume. 2. Angiotensinogen: A protein produced by the liver that's converted into angiotensin I by renin. 3. Angiotensin-Converting Enzyme (ACE): An enzyme that converts angiotensin I into 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, water retention, and potassium excretion. RAAS Activation: 1. Decreased blood pressure or volume is detected by the kidneys. 2. Renin is released, converting angiotensinogen into angiotensin I. 3. ACE converts angiotensin I into angiotensin II. 4. Angiotensin II stimulates the release of aldosterone, promoting sodium and water retention. 5. Blood pressure increases, and fluid balance is restored. Clinical Significance of RAAS: 1. Hypertension: Overactivation of RAAS can lead to high blood pressure. 2. Heart Failure: RAAS plays a crucial role in the development and progression of heart failure. 3. Kidney Disease: RAAS is involved in the pathogenesis of various kidney diseases, including diabetic nephropathy. 4. Fluid Balance Disorders: RAAS helps regulate fluid balance and electrolyte homeostasis.

Weldon ma

Weldon ma

Well done ma, it was well explanatory. Adebayo Mary Aanu, 2022000297, 400L. Nursing department

Renin Angiotensin Aldosterone System is an essential physiological mechanism, RAAS controls the body's fluid balance, blood pressure, and electrolyte balance. Important Elements of RAAS 1. Renin an enzyme that the kidneys release when blood volume or pressure drops. 2. Angiotensinogen: A liver-produced protein that renin transforms into angiotensin I. 3. The enzyme that changes angiotensin I into angiotensin ll is called angiotensin-converting enzyme (ACE). 4. Angiotensin II: A strong vasoconstrictor that raises blood pressure and causes aldosterone to be released. 5. Aldosterone: The adrenal glands create this hormone, which controls fluid balance and electrolyte balance. The RAAS Pathway 1. The release of Renin 2. Conversion of angiotensinogen to angiotensin I 3. Angiotensin I is changed into angiotensin I by ACE. 4. Angiotensin II promotes aldosterone and raises blood pressure. Olufojude Wuraola Oluwatobi 2023000665 Nursing, 300L

Great lecture ma, more power to your elbow ma. Thank and God bless.

Thanks ma 2023000711 Nursing 300L

Weldon ma

Great lecture

Well understood ma.

Weldon ma. Hassan Saulat Olanike 300L Nursing student 2023000478

renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood pressure, fluid balance, and electrolyte balance. It also controls the growth of tissues in the kidneys. How it works The kidneys release renin in response to changes in blood pressure, volume, and sodium and potassium levels. Renin cleaves angiotensinogen into angiotensin I. Angiotensin I is converted to angiotensin II. Angiotensin II stimulates the adrenal glands to release aldosterone. What it does The RAAS increases sodium and water reabsorption, and vascular tone. It also controls fluid and electrolyte balance by affecting the heart, blood vessels, and kidneys. What can happen if it's overactive? An overactive RAAS can lead to kidney disease. It can also cause hypertension, which can damage blood vessels and the glomerulus. Angiotensin II and aldosterone can also cause inflammation and fibrosis in the kidneys.

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Thanks for the lecture ma ADEBISI KUBURAT TOPE 300l Nursing Matric no 2023002084 RAAS is the system of hormones,proteins enezymes and reaction that regulates blood pressure and blood volume on a long term basis.

Esther onyinye obi 2023002076 300l Nursing Thank you ma for the lecture so far

RAAS stands for Renin-Angiotensin-Aldosterone System. It's a vital physiological pathway that regulates blood pressure, fluid balance, and electrolyte homeostasis in the body. Components of RAAS 1. _Renin_: An enzyme released by the kidneys in response to decreased blood pressure or low sodium levels. 2. _Angiotensinogen_: A protein produced by the liver, which is converted into angiotensin I by renin. 3. _Angiotensin-Converting Enzyme (ACE)_: An enzyme that converts angiotensin I into 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 regulates sodium and potassium balance, leading to increased blood pressure. Functions of RAAS 1. _Blood Pressure Regulation_: RAAS helps maintain blood pressure by constricting blood vessels and increasing fluid retention. 2. _Fluid Balance_: RAAS regulates fluid balance by controlling sodium and water reabsorption in the kidneys. 3. _Electrolyte Homeostasis_: RAAS helps maintain electrolyte balance by regulating sodium, potassium, and calcium levels. Dysregulation of RAAS Dysregulation of RAAS has been implicated in various diseases, including: 1. _Hypertension_: Overactivation of RAAS can lead to high blood pressure. 2. _Heart Failure_: RAAS dysregulation can contribute to the development and progression of heart failure. 3. _Kidney Disease_: RAAS dysregulation can lead to kidney damage and disease. 4. _Diabetes_: RAAS dysregulation can contribute to the development of diabetic nephropathy. Therapeutic Interventions Several therapeutic interventions target RAAS to manage diseases, including: 1. _ACE Inhibitors_: Block the conversion of angiotensin I to angiotensin II, reducing blood pressure and fluid retention. 2. _Angiotensin Receptor Blockers (ARBs)_: Block the action of angiotensin II on its receptors, reducing blood pressure and fluid retention. 3. _Aldosterone Antagonists_: Block the action of aldosterone, reducing fluid retention and blood pressure. 4. _Direct Renin Inhibitors_: Block the action of renin, reducing the production of angiotensin I and angiotensin II. Matric Number: 2023001655 Abdulrahman Ummulsalma Saidu 300l

Renin angiotensin system is a vital physiological pathway that regulates blood pressure, fluid balance and electrolytes homeostasis Components _Renin, Angiotensin,Angioy_converting enzyme _Angiotensin ii _Aldosterone Functions of RAS Blood pressure regulation Fluid balance Electrolyte homeostasis Deregulation of RAS causes the following _Hypeetension _Heart failure _kidney disease By Ajibowu Sariat Bidemi 2023001266

Thanks for the lecture ma

Sekoni Fauziat Atoke 2023000770 Nursing department 300 level

They will increase except calcium which is low

Sekoni Fauziat Atoke 2023000770 Nursing department 300 level

Sekoni Fauziat Atoke 2023000770 300 level Nursing department

Gray's tunner

The renin -angiotensin-adosterone system (RAAS) is a hormone system that controls blood pressure, fluid balance, and electrolyte levels. It's also involved in regulating vascular resistance. How it works The kidneys release renin in response to changes in blood pressure, sodium and potassium levels, and blood volume. Renin cleaves angiotensinogen, a protein in the plasma, into angiotensin I. Angiotensin I is then converted to angiotensin II. Angiotensin II stimulates the adrenal glands to release aldosterone. Aldosterone increases the reabsorption of sodium and water, and constricts blood vessels. What it's involved in Hypertension: The RAAS is a key target for treating hypertension. Uzondu Vera Chioma 2023000544 300l Nursing Dept

The Renin -Angiotensin Aldosterone System ( RAAS) is a physiological pathway that play a crucial role in regulating blood pressure, fluid balance, electrolyte balance, and fluid balance in the body. COMPONENTS OF RAAS ARE; 1. Renin:- an enzyme produced by the kidney that converts angiotensinogen to angiotensin 1. 2. Angiotensinogen:- is a protein produced by liver that serves as the substance for renin. 3. Angiotensin- converting enzyme (ACE):- is an enzyme found in the lungs that convert angiotensin I to angiotensin II. 4. Angiotensin II :- is a potent vasoconstrictor that increase blood pressure and stimulates the relaseo of aldosteron. 5. Aldosterone::- is a hormone produced by adrenal glands that regulate electrolyte and fluid balance. Raas has both physiological and pathological effecs on the body which are; Physiological effects 1. Blood pressure regulation 2. Fluid balance. 3. Electrolyte balance. Pathological effects are; 1.Hypertension 2.Heart failure. 3. Kidney disease. 4. Cardiovascular disease. 5. Fluid overload. Matric number : 2023002181

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Weldone ma

Welldone MA.... thanks for the wonderful and explanatory lecture ma... 2023001236 OLABAMIJI BARAKAT MAYOWA 300L NURSING SCIENCE

Thanks so much for the lecture ma SHITTU MARYAM OPEYEMI 2023001228 1. Ecchymosis is the bluish discoloration of the skin on the flank of the patient is called Grey Turner's sign 2) Cullein's sign is the bluish discoloration of the umbilicus due to internal bleeding cause by pancreatitis. 3) Increased glucose Increased amylase Calcium is decrease There is Also increase in lipase