Angiotensin II
Angiotensin II Type 1 Receptor Blockers
Receptor, Angiotensin, Type 1
Receptors, Angiotensin
Receptor, Angiotensin, Type 2
Angiotensin Receptor Antagonists
Losartan
Angiotensin I
Angiotensin-Converting Enzyme Inhibitors
Imidazoles
Renin-Angiotensin System
Antihypertensive Agents
Peptidyl-Dipeptidase A
Hypertension
Renin
Valine
Angiotensin III
Benzoates
Angiotensins
Rats, Sprague-Dawley
1-Sarcosine-8-Isoleucine Angiotensin II
Angiotensinogen
Pyridines
Kidney
Saralasin
Calcium Channel Blockers
Rats, Inbred SHR
Aldosterone
Enalapril
Rats, Inbred WKY
Dose-Response Relationship, Drug
Cells, Cultured
Rats, Wistar
RNA, Messenger
Myocardium
Disease Models, Animal
Cardiomegaly
Hypertension, Renal
Captopril
Amlodipine
Vasoconstriction
Bradykinin
Lisinopril
Fibrosis
Chymases
NADPH Oxidase
Signal Transduction
Mineralocorticoid Receptor Antagonists
Hemodynamics
Ramipril
Receptor, Bradykinin B2
Ventricular Remodeling
Spironolactone
Norepinephrine
Heart Failure
Drug Therapy, Combination
Mice, Knockout
Oxidative Stress
Nitric Oxide
Adrenergic beta-Antagonists
Hypertrophy
Diabetic Nephropathies
Enalaprilat
Receptors, Bradykinin
Sympathetic Nervous System
NG-Nitroarginine Methyl Ester
Kidney Glomerulus
Rats, Inbred Dahl
Enzyme Inhibitors
Calcium
Endothelin-1
Vascular Resistance
Atrial Natriuretic Factor
Kidney Tubules, Proximal
Vasodilation
Endothelium, Vascular
Aldosterone Synthase
Infusion Pumps, Implantable
Arrestins
Sodium
Aorta, Thoracic
Gene Expression Regulation
Teprotide
Hydrochlorothiazide
Analysis of Variance
Superoxides
Kinins
Adrenal Glands
Rabbits
Gene Expression
Glomerular Filtration Rate
Diet, Sodium-Restricted
Hypertrophy, Left Ventricular
Dihydropyridines
Immunohistochemistry
Blotting, Western
Body Weight
Reactive Oxygen Species
Myocardial Infarction
Up-Regulation
Nitric Oxide Synthase Type III
Nitric Oxide Synthase
Mesenteric Arteries
Dogs
Reverse Transcriptase Polymerase Chain Reaction
Phosphorylation
Angiotensin Amide
Potassium Channel Blockers
Myocytes, Cardiac
Heart Ventricles
Kidney Cortex
Azetidinecarboxylic Acid
Subfornical Organ
Enzyme Activation
Podocytes
Perindopril
Myocytes, Smooth Muscle
Endomyocardial Fibrosis
Diabetes Mellitus, Experimental
Receptors, G-Protein-Coupled
Protein Kinase C
Collagen
Collagen Type III
Transforming Growth Factor beta1
Nephrosclerosis
Polymorphism, Genetic
Treatment Outcome
Rats, Inbred Strains
Medulla Oblongata
Random Allocation
Vasopressins
Drug Interactions
Arterioles
Receptors, Endothelin
Chemokine CCL2
Receptors, Mineralocorticoid
Peptide Fragments
Transforming Growth Factor beta
Furosemide
Double-Blind Method
Diabetes Mellitus, Type 2
Phenylephrine
Receptor, Endothelin A
Mitogen-Activated Protein Kinases
Potassium
Nifedipine
Pre-Eclampsia
Arginine Vasopressin
Down-Regulation
Rats, Inbred OLETF
Amides
Baroreflex
Models, Animal
Blood Vessels
PPAR gamma
GTP-Binding Protein alpha Subunits, Gq-G11
Kidney Tubules
Indoles
Angiotensin receptor subtype 1 mediates angiotensin II enhancement of isoproterenol-induced cyclic AMP production in preglomerular microvascular smooth muscle cells. (1/1828)
In a previous study, we found that angiotensin (Ang) II enhances beta-adrenoceptor-induced cAMP production in cultured preglomerular microvascular smooth muscle cells (PMVSMCs) obtained from spontaneously hypertensive rats. The purpose of the present investigation was to identify the Ang receptor subtypes that mediate this effect. In our first study, we compared the ability of Ang II, Ang III, Ang (3-8), and Ang (1-7) to increase cAMP production in isoproterenol (1 microM)-treated PMVSMCs. Each peptide was tested at 0.1, 1, 10, 100, and 1000 nM. Both Ang II and Ang III increased intracellular (EC50s, 1 and 11 nM, respectively) and extracellular (EC50s, 2 and 14 nM, respectively) cAMP levels in a concentration-dependent fashion. In contrast, Ang (3-8) and Ang (1-7) did not enhance either intracellular or extracellular cAMP levels at any concentration tested. In our second study, we examined the ability of L 158809 [a selective Ang receptor subtype 1 (AT1) receptor antagonist] to inhibit Ang II (100 nM) and Ang III (100 nM) enhancement of isoproterenol (1 microM)-induced cAMP production in PMVSMCs. L 158809 (10 nM) abolished or nearly abolished (p <.001) Ang II and Ang III enhancement of isoproterenol-induced intracellular and extracellular cAMP levels. In contrast, PD 123319 (300 nM; a selective AT2 receptor antagonist) did not significantly alter Ang II enhancement of isoproterenol-induced intracellular or extracellular cAMP levels. We conclude that AT1 receptors, but not AT2, Ang (3-8), nor Ang (1-7) receptors mediate Ang II and Ang III enhancement of beta-adrenoceptor-induced cAMP production in cultured PMVSMCs. (+info)Angiotensin II antagonist prevents electrical remodeling in atrial fibrillation. (2/1828)
BACKGROUND: The blockade of angiotensin II (Ang II) formation has protective effects on cardiovascular tissue; however, the role of Ang II in atrial electrical remodeling is unknown. The purpose of this study was to investigate the effects of candesartan and captopril on atrial electrical remodeling. METHODS AND RESULTS: In 24 dogs, the atrial effective refractory period (AERP) was measured before, during, and after rapid atrial pacing. Rapid atrial pacing at 800 bpm was maintained for 180 minutes. The infusion of saline (n=8), candesartan (n=5), captopril (n=6), or Ang II (n=5) was initiated 30 minutes before rapid pacing and continued throughout the study. In the saline group, AERP was significantly shortened during rapid atrial pacing (from 149+/-11 to 132+/-16 ms, P<0.01). There was no significant difference in AERP shortening between the saline group and the Ang II group. However, in the candesartan and captopril groups, shortening of the AERP after rapid pacing was completely inhibited (from 142+/-9 to 147+/-12 ms with candesartan, from 153+/-15 to 153+/-14 ms with captopril, P=NS). Although rate adaptation of the AERP was lost in the saline group, this phenomenon was preserved in the candesartan and captopril groups. CONCLUSIONS: The inhibition of endogenous Ang II prevented AERP shortening during rapid atrial pacing. These results indicate for the first time that Ang II may be involved in the mechanism of atrial electrical remodeling and that the blockade of Ang II may lead to the better therapeutic management of human atrial fibrillation. (+info)Angiotensin II inhibits rat arterial KATP channels by inhibiting steady-state protein kinase A activity and activating protein kinase Ce. (3/1828)
We used whole-cell patch clamp to investigate steady-state activation of ATP-sensitive K+ channels (KATP) of rat arterial smooth muscle by protein kinase A (PKA) and the pathway by which angiotensin II (Ang II) inhibits these channels. Rp-cAMPS, an inhibitor of PKA, did not affect KATP currents activated by pinacidil when the intracellular solution contained 0.1 mM ATP. However, when ATP was increased to 1.0 mM, inhibition of PKA reduced KATP current, while the phosphatase inhibitor calyculin A caused a small increase in current. Ang II (100 nM) inhibited KATP current activated by the K+ channel opener pinacidil. The degree of inhibition was greater with 1.0 mM than with 0.1 mM intracellular ATP. The effect of Ang II was abolished by the AT1 receptor antagonist losartan. The inhibition of KATP currents by Ang II was abolished by a combination of PKA inhibitor peptide 5-24 (5 microM) and PKC inhibitor peptide 19-27 (100 microM), while either alone caused only partial block of the effect. In the presence of PKA inhibitor peptide, the inhibitory effect of Ang II was unaffected by the PKC inhibitor Go 6976, which is selective for Ca2+-dependent isoforms of PKC, but was abolished by a selective peptide inhibitor of the translocation of the epsilon isoform of PKC. Our results indicate that KATP channels are activated by steady-state phosphorylation by PKA at normal intracellular ATP levels, and that Ang II inhibits the channels both through activation of PKCepsilon and inhibition of PKA. (+info)Reactive oxygen species-mediated homologous downregulation of angiotensin II type 1 receptor mRNA by angiotensin II. (4/1828)
Recent studies suggest a crucial role of reactive oxygen species (ROS) for the signaling of angiotensin (Ang) II through Ang II type 1 receptor (AT(1)-R). However, the role of ROS in the regulation of AT(1)-R expression has not been explored. In this study, we examined the effect of an antioxidant on the homologous downregulation of AT(1)-R by Ang II. Ang II (10(-6) mol/L) decreased AT(1)-R mRNA with a peak suppression at 6 hours of stimulation in rat aortic vascular smooth muscle cells. Preincubation of vascular smooth muscle cells with N:-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT(1)-R mRNA. The effect of NAC was due to stabilization of the AT(1)-R mRNA that was destabilized by Ang II. The Ang II-induced AT(1)-R mRNA downregulation was also blocked by PD98059, an extracellular signal-regulated protein kinase (ERK) kinase inhibitor. Ang II-induced ERK activation was inhibited by NAC as well as by PD98059. Exogenous H(2)O(2) also suppressed AT(1)-R mRNA. These results suggest that the production of ROS and the activation of ERK are critical for the downregulation of AT(1)-R mRNA. The generation of ROS through stimulation of AT(1)-R not only mediates signaling of Ang II but also may play a crucial role in the adaptation process of AT(1)-R to the sustained stimulation of Ang II. (+info)Use of positron emission tomography to study AT1 receptor regulation in vivo. (5/1828)
Increased sodium intake and enhanced sodium sensitivity are implicated in the pathogenesis of hypertension and in the control of a major regulator of BP, the type 1 angiotensin receptor (AT(1) receptor). An in vivo technique to study changes of renal AT(1) receptors by dietary sodium was developed that uses positron emission tomography (PET). PET revealed that renal cortical AT(1) receptor binding was increased in sodium-loaded compared with sodium-deprived dogs, which correlated with ex vivo estimations of AT(1) receptor numbers. Plasma renin activity, angiotensin II, and aldosterone were inversely related to changes in AT(1) receptor binding. These results demonstrate, for the first time in vivo, that the renal AT(1) receptor is inversely related to the activity of the renin angiotensin system, which may provide a compensatory mechanism to prevent inappropriate fluctuations in arterial BP. The ability to measure AT(1) receptor binding in vivo has potential significance for clinical studies of AT(1) receptors, because PET is a noninvasive imaging technique that is readily applicable in humans. (+info)Angiotensin II type 1 and 2 receptors in conduit arteries of normal developing microswine. (6/1828)
OBJECTIVE: To identify vascular cells capable of responding to angiotensin II (Ang II) generated in conduit arteries, we examined the Ang II type 1 receptor (AT1R) and Ang II type 2 receptor (AT2R) in the thoracic aorta (TA) and abdominal aorta (AA) and branches in 90-day fetal, 3-week postnatal, and 6-month adult microswine. METHODS AND RESULTS: By autoradiography ((125)I-[Sar(1)Ile(8)]-Ang II with or without AT1R- or AT2R-selective analogues or (125)I-CGP 42112), there were striking rostrocaudal differences in (1) AT2R binding at all ages (prominent in AA wall and branches, sparse in TA wall and branches) and (2) a non-AT2R binding site for CGP 42112 (consistently evident in postnatal TA and branches but absent in AA and branches). Furthermore, patterns of AT2R distribution in infradiaphragmatic arteries were developmentally distinct. In fetal AAs, high-density AT2Rs occupied the inner 60% of the medial-endothelial wall. In postnatal AAs, AT2Rs were sparse in the medial-endothelial wall but prominent in a circumferential smooth muscle alpha-actin-negative cell layer at the medial-adventitial border, occupying approximately 20% to 25% of the AA cross-sectional area. AT1R density in the TA and AA medial-endothelial wall increased with age, whereas AT2R density decreased after birth. CONCLUSIONS: A novel AT2R-positive cell layer confined to postnatal infradiaphragmatic arteries physically links adventitial and medial layers, appears optimally positioned to transduce AT2R-dependent functions of local Ang II, and suggests that adventitial Ang II may elicit regionally distinct vascular responses. (+info)Angiotensin II type 1 receptor blockade to control blood pressure in postmenopausal women: influence of hormone replacement therapy. (7/1828)
BACKGROUND: Hypertension is twice as common in postmenopausal than in premenopausal women. This study evaluated the effectiveness of a blockade of the renin-angiotensin-aldosterone system (RAAS) with candesartan cilexetil (CC) to control blood pressure (BP) in hypertensive menopausal women, and the influence of hormone replacement therapy (HRT). METHODS: This was designed as a prospective, open-label and non-comparative study. Included were 618 hypertensive menopausal women grade I/II according to the Sixth Report of the Joint National Committee (VI-JNC), with an average age 52+/-4.7 years (95% CI 52.3-53.0) and with a last menstrual period (LMP) at least one year before. BP was determined by measurement in four visits during six months of follow-up, according to the recommendations of the OMS/SIH. Optimal control of BP was considered as BP <140/90 mm Hg. RESULTS: A statistically significant decrease in systolic (SBP; 19.9+/-11.2) and diastolic (DBP; 11.5+/-7.3) blood pressure mm Hg values was observed (P<0.01). The control of BP increased significantly over time to 61.2% (P<0.01). In multivariate analysis, only age was associated with control of BP (beta= -0.062; P=0.004). Of the women not controlled in the second visit, 12.5 mg of hydrochlorothiazide (HCTZ) were added to 31.5% (N=122), with 80% more BP control achieved in visit 3 than in the non-supplement group (OR=1.8; 95% CI 1.04-3.05; P<0.03). One hundred and three (16.7%) patients were receiving HRT for 2.01+/-2.23 years (95% CI 1.55-2.46). HRT did not affect the control of BP. No severe adverse reactions were reported. CONCLUSIONS: Candesartan cilexetil significantly reduced SBP and DBP and increased control (61.2%) of BP in hypertensive menopausal women. Only age had an inverse association with control of BP. In this study, HRT did not affect the control of BP. (+info)Effects of dual blockade of the renin-angiotensin system in primary proteinuric nephropathies. (8/1828)
BACKGROUND: Blockade of the renin-angiotensin system (RAS) with angiotensin converting enzyme (ACE) inhibitors or with angiotensin II type 1 (AT1) receptor blockers has been shown to reduce proteinuria and to slow down the progression of renal disease in diabetic and non-diabetic primary proteinuric nephropathies. Additionally, this beneficial effect is not dependent on blood pressure control. METHODS: To assess and compare the effects of lisinopril (up to 40 mg/day), candesartan (up to 32 mg/day) and combination therapy (lisinopril up to 20 mg/day plus candesartan up to 16 mg/day) on urinary protein excretion, 45 patients with primary proteinuric nephropathies (urinary protein/creatinine ratio 3.8+/-2.4 g/g) and normal or slightly reduced renal function (CCr 95+/-33 mL/min) were enrolled in a six month multicenter, prospective, open, randomized, active-controlled and parallel-group trial with 1:1:1 allocation. Blood pressure goal was set at or below 125/75 mm Hg for all patients, with additional antihypertensive medication prescribed if required. RESULTS: Renal function, estimated by creatinine clearance, remained stable throughout the study. Hyperkalemia (K>5.5 mmol/L) was detected in 3.1% of all measurements in follow-up, and was more frequent in patients treated with lisinopril alone or lisinopril plus candesartan (P<0.001) than in those on candesartan alone. No other relevant adverse event was recorded. The blood pressure goal (<125/75 mm Hg) was achieved by week 4 in all treatment groups (P<0.005 when compared to baseline), and afterwards the mean systolic and diastolic blood pressure remained below these values until the end of the trial with no statistically significant differences between groups. Urinary protein/creatinine ratio (percentage reduction 95% confidence intervals CI) decreased in patients treated with lisinopril alone to -33% (CI -12-56) to -31% (CI 0-68) and to -50% (CI -9-90), in patients treated with candesartan to -28% (CI -12-45), to -41% (CI -30-52) and to -48% (CI -32-63), in patients treated with the combination of both to -60% (CI -44-77) to -54% (CI -38-69) and to -70% (CI -57-83) at two, three, and six months, respectively. All comparisons with baseline achieved statistical significance and treatment with combination therapy was statistically more effective in proteinuria reduction than treatment with candesartan alone at two and six months (P=0.004 and P=0.023, respectively) and than treatment with lisinopril only at two months (P=0.03). CONCLUSION: Dual blockade of the renin-angiotensin system with ACE inhibitors and AT1 receptor blockers produces a beneficial antiproteinuric effect that could not be explained only by the systemic blood pressure reduction. All treatments were well tolerated. (+info)There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Medical Term: Cardiomegaly
Definition: An abnormal enlargement of the heart.
Symptoms: Difficulty breathing, shortness of breath, fatigue, swelling of legs and feet, chest pain, and palpitations.
Causes: Hypertension, cardiac valve disease, myocardial infarction (heart attack), congenital heart defects, and other conditions that affect the heart muscle or cardiovascular system.
Diagnosis: Physical examination, electrocardiogram (ECG), chest x-ray, echocardiography, and other diagnostic tests as necessary.
Treatment: Medications such as diuretics, vasodilators, and beta blockers, lifestyle changes such as exercise and diet modifications, surgery or other interventions in severe cases.
Note: Cardiomegaly is a serious medical condition that requires prompt diagnosis and treatment to prevent complications such as heart failure and death. If you suspect you or someone else may have cardiomegaly, seek medical attention immediately.
A type of hypertension that is caused by a problem with the kidneys. It can be acute or chronic and may be associated with other conditions such as glomerulonephritis, pyelonephritis, or polycystic kidney disease. Symptoms include proteinuria, hematuria, and elevated blood pressure. Treatment options include diuretics, ACE inhibitors, and angiotensin II receptor blockers.
Note: Renal hypertension is also known as renal artery hypertension.
Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.
Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.
Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.
There are many different types of fibrosis, including:
* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.
Fibrosis can be diagnosed through a variety of methods, including:
* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.
There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:
* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.
It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.
During ventricular remodeling, the heart muscle becomes thicker and less flexible, leading to a decrease in the heart's ability to fill with blood and pump it out to the body. This can lead to shortness of breath, fatigue, and swelling in the legs and feet.
Ventricular remodeling is a natural response to injury, but it can also be exacerbated by factors such as high blood pressure, diabetes, and obesity. Treatment for ventricular remodeling typically involves medications and lifestyle changes, such as exercise and a healthy diet, to help manage symptoms and slow the progression of the condition. In some cases, surgery or other procedures may be necessary to repair or replace damaged heart tissue.
The process of ventricular remodeling is complex and involves multiple cellular and molecular mechanisms. It is thought to be driven by a variety of factors, including changes in gene expression, inflammation, and the activity of various signaling pathways.
Overall, ventricular remodeling is an important condition that can have significant consequences for patients with heart disease. Understanding its causes and mechanisms is crucial for developing effective treatments and improving outcomes for those affected by this condition.
There are two main types of heart failure:
1. Left-sided heart failure: This occurs when the left ventricle, which is the main pumping chamber of the heart, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the lungs and other organs.
2. Right-sided heart failure: This occurs when the right ventricle, which pumps blood to the lungs, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the body's tissues and organs.
Symptoms of heart failure may include:
* Shortness of breath
* Fatigue
* Swelling in the legs, ankles, and feet
* Swelling in the abdomen
* Weight gain
* Coughing up pink, frothy fluid
* Rapid or irregular heartbeat
* Dizziness or lightheadedness
Treatment for heart failure typically involves a combination of medications and lifestyle changes. Medications may include diuretics to remove excess fluid from the body, ACE inhibitors or beta blockers to reduce blood pressure and improve blood flow, and aldosterone antagonists to reduce the amount of fluid in the body. Lifestyle changes may include a healthy diet, regular exercise, and stress reduction techniques. In severe cases, heart failure may require hospitalization or implantation of a device such as an implantable cardioverter-defibrillator (ICD) or a left ventricular assist device (LVAD).
It is important to note that heart failure is a chronic condition, and it requires ongoing management and monitoring to prevent complications and improve quality of life. With proper treatment and lifestyle changes, many people with heart failure are able to manage their symptoms and lead active lives.
There are several types of hypertrophy, including:
1. Muscle hypertrophy: The enlargement of muscle fibers due to increased protein synthesis and cell growth, often seen in individuals who engage in resistance training exercises.
2. Cardiac hypertrophy: The enlargement of the heart due to an increase in cardiac workload, often seen in individuals with high blood pressure or other cardiovascular conditions.
3. Adipose tissue hypertrophy: The excessive growth of fat cells, often seen in individuals who are obese or have insulin resistance.
4. Neurological hypertrophy: The enlargement of neural structures such as brain or spinal cord due to an increase in the number of neurons or glial cells, often seen in individuals with neurodegenerative diseases such as Alzheimer's or Parkinson's.
5. Hepatic hypertrophy: The enlargement of the liver due to an increase in the number of liver cells, often seen in individuals with liver disease or cirrhosis.
6. Renal hypertrophy: The enlargement of the kidneys due to an increase in blood flow and filtration, often seen in individuals with kidney disease or hypertension.
7. Ovarian hypertrophy: The enlargement of the ovaries due to an increase in the number of follicles or hormonal imbalances, often seen in individuals with polycystic ovary syndrome (PCOS).
Hypertrophy can be diagnosed through various medical tests such as imaging studies (e.g., CT scans, MRI), biopsies, and blood tests. Treatment options for hypertrophy depend on the underlying cause and may include medications, lifestyle changes, and surgery.
In conclusion, hypertrophy is a growth or enlargement of cells, tissues, or organs in response to an excessive stimulus. It can occur in various parts of the body, including the brain, liver, kidneys, heart, muscles, and ovaries. Understanding the underlying causes and diagnosis of hypertrophy is crucial for effective treatment and management of related health conditions.
There are several types of diabetic nephropathy, including:
1. Mesangial proliferative glomerulonephritis: This is the most common type of diabetic nephropathy and is characterized by an overgrowth of cells in the mesangium, a part of the glomerulus (the blood-filtering unit of the kidney).
2. Segmental sclerosis: This type of diabetic nephropathy involves the hardening of some parts of the glomeruli, leading to decreased kidney function.
3. Fibrotic glomerulopathy: This is a rare form of diabetic nephropathy that is characterized by the accumulation of fibrotic tissue in the glomeruli.
4. Membranous nephropathy: This type of diabetic nephropathy involves the deposition of immune complexes (antigen-antibody complexes) in the glomeruli, leading to inflammation and damage to the kidneys.
5. Minimal change disease: This is a rare form of diabetic nephropathy that is characterized by minimal changes in the glomeruli, but with significant loss of kidney function.
The symptoms of diabetic nephropathy can be non-specific and may include proteinuria (excess protein in the urine), hematuria (blood in the urine), and decreased kidney function. Diagnosis is typically made through a combination of physical examination, medical history, laboratory tests, and imaging studies such as ultrasound or CT scans.
Treatment for diabetic nephropathy typically involves managing blood sugar levels through lifestyle changes (such as diet and exercise) and medication, as well as controlling high blood pressure and other underlying conditions. In severe cases, dialysis or kidney transplantation may be necessary. Early detection and management of diabetic nephropathy can help slow the progression of the disease and improve outcomes for patients with this condition.
Symptoms of renovascular hypertension may include:
* High blood pressure that is resistant to treatment
* Flank pain or back pain
* Hematuria (blood in the urine)
* Proteinuria (excess protein in the urine)
* Decreased kidney function
Diagnosis of renovascular hypertension typically involves imaging tests such as angiography, CT or MRI angiography, or ultrasound to evaluate the renal arteries and identify any blockages or narrowing. Other tests such as arenography, captopril test, or adrenomedullin testing may also be used to support the diagnosis.
Treatment of renovascular hypertension typically involves medications to lower blood pressure, such as beta blockers, ACE inhibitors, or calcium channel blockers. In some cases, surgery may be necessary to restore blood flow to the kidneys. For example, atherosclerosis can be treated with angioplasty or bypass surgery.
It is important to note that renovascular hypertension is a relatively rare cause of hypertension and only accounts for about 5-10% of all cases of hypertension. However, it is an important differential diagnosis for hypertension that is resistant to treatment or has a sudden onset.
Albuminuria is often associated with conditions such as diabetes, high blood pressure, and kidney disease, as these conditions can damage the kidneys and cause albumin to leak into the urine. It is also a common finding in people with chronic kidney disease (CKD), as the damaged kidneys are unable to filter out the excess protein.
If left untreated, albuminuria can lead to complications such as kidney failure, cardiovascular disease, and an increased risk of death. Treatment options for albuminuria include medications to lower blood pressure and control blood sugar levels, as well as dietary changes and lifestyle modifications. In severe cases, dialysis or kidney transplantation may be necessary.
In summary, albuminuria is the presence of albumin in the urine, which can be an indicator of kidney damage or disease. It is often associated with conditions such as diabetes and high blood pressure, and can lead to complications if left untreated.
LVH can lead to a number of complications, including:
1. Heart failure: The enlarged left ventricle can become less efficient at pumping blood throughout the body, leading to heart failure.
2. Arrhythmias: The abnormal electrical activity in the heart can lead to irregular heart rhythms.
3. Sudden cardiac death: In some cases, LVH can increase the risk of sudden cardiac death.
4. Atrial fibrillation: The enlarged left atrium can lead to atrial fibrillation, a common type of arrhythmia.
5. Mitral regurgitation: The enlargement of the left ventricle can cause the mitral valve to become incompetent, leading to mitral regurgitation.
6. Heart valve problems: The enlarged left ventricle can lead to heart valve problems, such as mitral regurgitation or aortic stenosis.
7. Coronary artery disease: LVH can increase the risk of coronary artery disease, which can lead to a heart attack.
8. Pulmonary hypertension: The enlarged left ventricle can lead to pulmonary hypertension, which can further strain the heart and increase the risk of complications.
Evaluation of LVH typically involves a physical examination, medical history, electrocardiogram (ECG), echocardiography, and other diagnostic tests such as stress test or cardiac MRI. Treatment options for LVH depend on the underlying cause and may include medications, lifestyle changes, and in some cases, surgery or other interventions.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
There are different types of myocardial infarctions, including:
1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.
Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.
Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.
Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.
Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.
Types of Kidney Diseases:
1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.
Symptoms of Kidney Diseases:
1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss
Diagnosis of Kidney Diseases:
1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)
Treatment of Kidney Diseases:
1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)
Prevention of Kidney Diseases:
1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings
Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.
The exact cause of endomyocardial fibrosis is not known, but it is believed to be related to inflammation and scarring within the heart. The condition is more common in men than women, and typically affects people between the ages of 20 and 50. Symptoms of endomyocardial fibrosis can include shortness of breath, fatigue, swelling in the legs and feet, and chest pain.
There is no cure for endomyocardial fibrosis, but treatment options may include medications to manage symptoms, surgery to repair or replace damaged heart tissue, and lifestyle changes such as a healthy diet and regular exercise. In severe cases, heart transplantation may be necessary. Early diagnosis and treatment can help slow the progression of the condition and improve quality of life for those affected.
Types of Experimental Diabetes Mellitus include:
1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.
Experimental Diabetes Mellitus has several applications in research, including:
1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.
In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.
Nephrosclerosis can be caused by a variety of factors, including:
1. Diabetes: High blood sugar levels over an extended period can damage the kidney tissues and lead to nephrosclerosis.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the kidney blood vessels, leading to scarring and hardening of the tissues.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood, can lead to nephrosclerosis.
4. Obesity: Excess weight can increase the risk of developing diabetes and hypertension, both of which are leading causes of nephrosclerosis.
5. Family history: A family history of kidney disease increases the risk of developing nephrosclerosis.
6. Certain medications: Long-term use of certain medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and certain antibiotics can damage the kidneys and lead to nephrosclerosis.
7. Infections: Certain infections, such as pyelonephritis, can spread to the kidneys and cause inflammation and scarring that leads to nephrosclerosis.
8. Kidney stones: Recurring kidney stones can cause chronic inflammation and damage to the kidney tissues, leading to nephrosclerosis.
9. Certain medical conditions: Certain medical conditions, such as systemic lupus erythematosus and vasculitis, can increase the risk of developing nephrosclerosis.
Symptoms of nephrosclerosis may include:
1. Proteinuria: Excess protein in the urine.
2. Hematuria: Blood in the urine.
3. Reduced kidney function: Decreased ability of the kidneys to filter waste and excess fluids from the blood.
4. High blood pressure: Hypertension is common in people with nephrosclerosis.
5. Swelling: Fluid retention in the legs, ankles, and feet.
6. Fatigue: Weakness and tiredness due to the buildup of waste products in the body.
7. Nausea and vomiting: Due to the buildup of waste products in the body.
8. Skin rash: Some people with nephrosclerosis may develop a skin rash.
Nephrosclerosis can be diagnosed through a combination of physical examination, medical history, urine and blood tests, and imaging studies such as ultrasound and CT scans. Treatment for nephrosclerosis depends on the underlying cause and may include medications to control high blood pressure, reduce proteinuria, and slow the progression of the disease. In severe cases, dialysis or kidney transplantation may be necessary.
It is essential to seek medical attention if you experience any symptoms of nephrosclerosis, as early diagnosis and treatment can help prevent complications and improve outcomes. A healthcare professional can perform a physical examination, take a medical history, and order diagnostic tests to determine the underlying cause of your symptoms. Based on the severity and underlying cause of your condition, a treatment plan will be developed that may include medications, lifestyle modifications, or dialysis. With proper treatment, many people with nephrosclerosis can manage their symptoms and improve their quality of life.
Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.
Common symptoms of type 2 diabetes include:
* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections
If left untreated, type 2 diabetes can lead to a range of complications, including:
* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation
The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:
* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.
There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.
There are several types of pre-eclampsia, including:
1. Mild pre-eclampsia: This type is characterized by mild high blood pressure and no damage to organs.
2. Severe pre-eclampsia: This type is characterized by severe high blood pressure and damage to organs such as the liver and kidneys.
3. Eclampsia: This is a more severe form of pre-eclampsia that is characterized by seizures or coma.
Pre-eclampsia can be caused by several factors, including:
1. Poor blood flow to the placenta
2. Immune system problems
3. Hormonal imbalances
4. Genetic mutations
5. Nutritional deficiencies
Pre-eclampsia can be diagnosed through several tests, including:
1. Blood pressure readings
2. Urine tests to check for protein and other substances
3. Ultrasound exams to assess fetal growth and well-being
4. Blood tests to check liver and kidney function
There is no cure for pre-eclampsia, but it can be managed through several strategies, including:
1. Close monitoring of the mother and baby
2. Medications to lower blood pressure and prevent seizures
3. Bed rest or hospitalization
4. Delivery, either vaginal or cesarean
Pre-eclampsia can be a challenging condition to manage, but with proper care and close monitoring, the risk of complications can be reduced. It is essential for pregnant women to receive regular prenatal care and report any symptoms promptly to their healthcare provider. Early detection and management of pre-eclampsia can help ensure a healthy pregnancy outcome for both the mother and the baby.
The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.
In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.
What is a Chronic Disease?
A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:
1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke
Impact of Chronic Diseases
The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.
Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.
Addressing Chronic Diseases
Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:
1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.
Conclusion
Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.
Causes of Hyperkalemia:
1. Kidney dysfunction: When the kidneys are not able to excrete excess potassium, it can build up in the bloodstream and lead to hyperkalemia.
2. Medications: Certain drugs, such as ACE inhibitors, potassium-sparing diuretics, and NSAIDs, can increase potassium levels by blocking the excretion of potassium in the urine.
3. Diabetic ketoacidosis: High levels of potassium can occur in people with uncontrolled diabetes who have diabetic ketoacidosis.
4. Acute kidney injury: This condition can cause a rapid increase in potassium levels as the kidneys are unable to remove excess potassium from the blood.
5. Heart disease: Potassium levels can rise in people with heart failure or other cardiac conditions, leading to hyperkalemia.
Symptoms of Hyperkalemia:
1. Muscle weakness and fatigue
2. Abnormal heart rhythms (arrhythmias)
3. Palpitations
4. Constipation
5. Nausea and vomiting
6. Abdominal cramps
7. Fatigue
8. Confusion
9. Headaches
10. Weakness in the legs and feet
Treatment of Hyperkalemia:
The treatment of hyperkalemia depends on the underlying cause and the severity of the condition. Some of the common methods for lowering potassium levels include:
1. Diuretics: These medications help remove excess fluid and electrolytes, including potassium, from the body.
2. Calcium gluconate: This medication can help stabilize cardiac function and reduce the risk of arrhythmias.
3. Insulin and glucose: Giving insulin and glucose to someone with diabetic ketoacidosis can help lower potassium levels by increasing glucose uptake in the cells.
4. Hemodialysis: This is a process that uses a machine to filter waste products, including excess potassium, from the blood.
5. Potassium-binding resins: These medications can bind to potassium ions in the gut and prevent their absorption into the bloodstream.
6. Sodium polystyrene sulfonate (Kayexalate): This medication can help lower potassium levels by binding to excess potassium in the gut and causing it to be eliminated in the stool.
7. Activated charcoal: This medication can help bind to potassium ions in the gut and prevent their absorption into the bloodstream.
In severe cases of hyperkalemia, hospitalization may be necessary to monitor and treat the condition. In some instances, dialysis may be required to remove excess potassium from the blood. It is important to note that the treatment for hyperkalemia should only be done under the guidance of a healthcare professional, as some medications or procedures can worsen the condition if not properly managed.
Treatment for ureteral obstruction depends on the underlying cause and may include medications, endoscopic procedures, or surgery. In some cases, a temporary drainage catheter may be placed in the ureter to help relieve symptoms until the blockage can be fully treated.
Ureteral obstruction can be acute or chronic, and may occur in adults or children. It is important to seek medical attention if symptoms persist or worsen over time, as untreated ureteral obstruction can lead to complications such as kidney damage or sepsis.
Causes of Ureteral Obstruction:
Ureteral obstruction can be caused by a variety of factors, including:
1. Kidney stones: Small, hard mineral deposits that form in the urine and can block the flow of urine through the ureters.
2. Tumors: Cancerous or non-cancerous growths that can block the ureters.
3. Scar tissue: Scarring from previous surgeries or injuries can cause narrowing or blockages in the ureters.
4. Prostate enlargement: In men, an enlarged prostate gland can press on the urethra and ureters, causing blockages.
5. Bladder neck obstruction: A condition where the bladder neck is narrow or blocked, preventing urine from flowing through the urethra.
6. Trauma: Injuries to the ureters or bladder can cause blockages.
7. Inflammation: Inflammation in the ureters or kidneys can cause swelling and blockages.
8. Congenital conditions: Some people may be born with abnormalities that cause blockages in the urinary tract.
9. Neurological disorders: Conditions such as multiple sclerosis, Parkinson's disease, or spinal cord injuries can affect the nerves that control the bladder and ureters, leading to blockages.
10. Medications: Certain medications, such as certain antibiotics and chemotherapy drugs, can cause damage to the ureters and lead to blockages.
A condition in which the kidneys gradually lose their function over time, leading to the accumulation of waste products in the body. Also known as chronic kidney disease (CKD).
Prevalence:
Chronic kidney failure affects approximately 20 million people worldwide and is a major public health concern. In the United States, it is estimated that 1 in 5 adults has CKD, with African Americans being disproportionately affected.
Causes:
The causes of chronic kidney failure are numerous and include:
1. Diabetes: High blood sugar levels can damage the kidneys over time.
2. Hypertension: Uncontrolled high blood pressure can cause damage to the blood vessels in the kidneys.
3. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste and excess fluids from the blood.
4. Interstitial nephritis: Inflammation of the tissue between the kidney tubules.
5. Pyelonephritis: Infection of the kidneys, usually caused by bacteria or viruses.
6. Polycystic kidney disease: A genetic disorder that causes cysts to grow on the kidneys.
7. Obesity: Excess weight can increase blood pressure and strain on the kidneys.
8. Family history: A family history of kidney disease increases the risk of developing chronic kidney failure.
Symptoms:
Early stages of chronic kidney failure may not cause any symptoms, but as the disease progresses, symptoms can include:
1. Fatigue: Feeling tired or weak.
2. Swelling: In the legs, ankles, and feet.
3. Nausea and vomiting: Due to the buildup of waste products in the body.
4. Poor appetite: Loss of interest in food.
5. Difficulty concentrating: Cognitive impairment due to the buildup of waste products in the brain.
6. Shortness of breath: Due to fluid buildup in the lungs.
7. Pain: In the back, flank, or abdomen.
8. Urination changes: Decreased urine production, dark-colored urine, or blood in the urine.
9. Heart problems: Chronic kidney failure can increase the risk of heart disease and heart attack.
Diagnosis:
Chronic kidney failure is typically diagnosed based on a combination of physical examination findings, medical history, laboratory tests, and imaging studies. Laboratory tests may include:
1. Blood urea nitrogen (BUN) and creatinine: Waste products in the blood that increase with decreased kidney function.
2. Electrolyte levels: Imbalances in electrolytes such as sodium, potassium, and phosphorus can indicate kidney dysfunction.
3. Kidney function tests: Measurement of glomerular filtration rate (GFR) to determine the level of kidney function.
4. Urinalysis: Examination of urine for protein, blood, or white blood cells.
Imaging studies may include:
1. Ultrasound: To assess the size and shape of the kidneys, detect any blockages, and identify any other abnormalities.
2. Computed tomography (CT) scan: To provide detailed images of the kidneys and detect any obstructions or abscesses.
3. Magnetic resonance imaging (MRI): To evaluate the kidneys and detect any damage or scarring.
Treatment:
Treatment for chronic kidney failure depends on the underlying cause and the severity of the disease. The goals of treatment are to slow progression of the disease, manage symptoms, and improve quality of life. Treatment may include:
1. Medications: To control high blood pressure, lower cholesterol levels, reduce proteinuria, and manage anemia.
2. Diet: A healthy diet that limits protein intake, controls salt and water intake, and emphasizes low-fat dairy products, fruits, and vegetables.
3. Fluid management: Monitoring and control of fluid intake to prevent fluid buildup in the body.
4. Dialysis: A machine that filters waste products from the blood when the kidneys are no longer able to do so.
5. Transplantation: A kidney transplant may be considered for some patients with advanced chronic kidney failure.
Complications:
Chronic kidney failure can lead to several complications, including:
1. Heart disease: High blood pressure and anemia can increase the risk of heart disease.
2. Anemia: A decrease in red blood cells can cause fatigue, weakness, and shortness of breath.
3. Bone disease: A disorder that can lead to bone pain, weakness, and an increased risk of fractures.
4. Electrolyte imbalance: Imbalances of electrolytes such as potassium, phosphorus, and sodium can cause muscle weakness, heart arrhythmias, and other complications.
5. Infections: A decrease in immune function can increase the risk of infections.
6. Nutritional deficiencies: Poor appetite, nausea, and vomiting can lead to malnutrition and nutrient deficiencies.
7. Cardiovascular disease: High blood pressure, anemia, and other complications can increase the risk of cardiovascular disease.
8. Pain: Chronic kidney failure can cause pain, particularly in the back, flank, and abdomen.
9. Sleep disorders: Insomnia, sleep apnea, and restless leg syndrome are common complications.
10. Depression and anxiety: The emotional burden of chronic kidney failure can lead to depression and anxiety.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
There are several potential causes of LVD, including:
1. Coronary artery disease: The buildup of plaque in the coronary arteries can lead to a heart attack, which can damage the left ventricle and impair its ability to function properly.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, it can lead to LVD.
3. Cardiomyopathy: This is a condition where the heart muscle becomes weakened or enlarged, leading to impaired function of the left ventricle.
4. Heart valve disease: Problems with the heart valves can disrupt the normal flow of blood and cause LVD.
5. Hypertension: High blood pressure can cause damage to the heart muscle and lead to LVD.
6. Genetic factors: Some people may be born with genetic mutations that predispose them to developing LVD.
7. Viral infections: Certain viral infections, such as myocarditis, can inflame and damage the heart muscle, leading to LVD.
8. Alcohol or drug abuse: Substance abuse can damage the heart muscle and lead to LVD.
9. Nutritional deficiencies: A diet lacking essential nutrients can lead to damage to the heart muscle and increase the risk of LVD.
Diagnosis of LVD typically involves a physical exam, medical history, and results of diagnostic tests such as electrocardiograms (ECGs), echocardiograms, and stress tests. Treatment options for LVD depend on the underlying cause, but may include medications to improve cardiac function, lifestyle changes, and in severe cases, surgery or other procedures.
Preventing LVD involves taking steps to maintain a healthy heart and reducing risk factors such as high blood pressure, smoking, and obesity. This can be achieved through a balanced diet, regular exercise, stress management, and avoiding substance abuse. Early detection and treatment of underlying conditions that increase the risk of LVD can also help prevent the condition from developing.
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.
There are several types of myocardial ischemia, including:
1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.
Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.
The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.
The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.
Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.
Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.
In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.
1. Coronary artery disease: The narrowing or blockage of the coronary arteries, which supply blood to the heart.
2. Heart failure: A condition in which the heart is unable to pump enough blood to meet the body's needs.
3. Arrhythmias: Abnormal heart rhythms that can be too fast, too slow, or irregular.
4. Heart valve disease: Problems with the heart valves that control blood flow through the heart.
5. Heart muscle disease (cardiomyopathy): Disease of the heart muscle that can lead to heart failure.
6. Congenital heart disease: Defects in the heart's structure and function that are present at birth.
7. Peripheral artery disease: The narrowing or blockage of blood vessels that supply oxygen and nutrients to the arms, legs, and other organs.
8. Deep vein thrombosis (DVT): A blood clot that forms in a deep vein, usually in the leg.
9. Pulmonary embolism: A blockage in one of the arteries in the lungs, which can be caused by a blood clot or other debris.
10. Stroke: A condition in which there is a lack of oxygen to the brain due to a blockage or rupture of blood vessels.
MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.
The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.
The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.
The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.
Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.
In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.
There are several factors that can contribute to the development of insulin resistance, including:
1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.
There are several ways to diagnose insulin resistance, including:
1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.
There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:
1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.
Medications that may be used to treat insulin resistance include:
1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.
It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.
Symptoms of PIH can include:
* Headaches
* Blurred vision
* Nausea and vomiting
* Abdominal pain
* Swelling of the hands and feet
* Shortness of breath
* Seizures (in severe cases)
PIH can be diagnosed through blood pressure readings, urine tests, and imaging studies such as ultrasound. Treatment for PIH usually involves bed rest, medication to lower blood pressure, and close monitoring by a healthcare provider. In severe cases, delivery may be necessary.
Preventive measures for PIH include:
* Regular prenatal care to monitor blood pressure and detect any changes early
* Avoiding excessive weight gain during pregnancy
* Eating a healthy diet low in salt and fat
* Getting regular exercise as recommended by a healthcare provider
PIH can be a serious condition for both the mother and the baby. If left untreated, it can lead to complications such as stroke, placental abruption (separation of the placenta from the uterus), and premature birth. In severe cases, it can be life-threatening for both the mother and the baby.
Overall, PIH is a condition that requires close monitoring and careful management to ensure a healthy pregnancy outcome.
The symptoms of Marfan syndrome can vary widely among individuals with the condition, but typically include:
1. Tall stature (often over 6 feet 5 inches)
2. Long limbs and fingers
3. Curvature of the spine (scoliosis)
4. Flexible joints
5. Eye problems, such as nearsightedness, glaucoma, and detached retinas
6. Heart problems, such as mitral valve prolapse and aortic dilatation
7. Blood vessel problems, such as aneurysms and dissections
8. Lung problems, such as pneumothorax (collapsed lung)
9. Other skeletal problems, such as pectus excavatum (a depression in the chest wall) and clubfoot
Marfan syndrome is usually diagnosed through a combination of clinical evaluation, family history, and genetic testing. Treatment for the condition typically involves managing its various symptoms and complications, such as with medication, surgery, or lifestyle modifications. Individuals with Marfan syndrome may also need to avoid activities that could exacerbate their condition, such as contact sports or heavy lifting.
While there is currently no cure for Marfan syndrome, early diagnosis and appropriate management can help individuals with the condition live long and relatively healthy lives. With proper care and attention, many people with Marfan syndrome are able to lead fulfilling lives and achieve their goals.
Symptoms of hydronephrosis may include flank pain, nausea, vomiting, fever, and blood in the urine. If left untreated, hydronephrosis can lead to kidney damage and even failure. Treatment for hydronephrosis typically involves relieving the obstruction and addressing any underlying causes. In some cases, surgery may be necessary to repair damaged tissue or remove blockages.
Hydronephrosis is a serious medical condition that requires prompt medical attention to prevent complications and preserve kidney function. It is important to seek medical care if symptoms of hydronephrosis are present, as early diagnosis and treatment can improve outcomes.
Measurement:
Cardiac output is typically measured using invasive or non-invasive methods. Invasive methods involve inserting a catheter into the heart to directly measure cardiac output. Non-invasive methods include echocardiography, MRI, and CT scans. These tests can provide an estimate of cardiac output based on the volume of blood being pumped out of the heart and the rate at which it is being pumped.
Causes:
There are several factors that can contribute to low cardiac output. These include:
1. Heart failure: This occurs when the heart is unable to pump enough blood to meet the body's needs, leading to fatigue and shortness of breath.
2. Anemia: A low red blood cell count can reduce the amount of oxygen being delivered to the body's tissues, leading to fatigue and weakness.
3. Medication side effects: Certain medications, such as beta blockers, can slow down the heart rate and reduce cardiac output.
4. Sepsis: A severe infection can lead to inflammation throughout the body, which can affect the heart's ability to pump blood effectively.
5. Myocardial infarction (heart attack): This occurs when the heart muscle is damaged due to a lack of oxygen, leading to reduced cardiac output.
Symptoms:
Low cardiac output can cause a range of symptoms, including:
1. Fatigue and weakness
2. Dizziness and lightheadedness
3. Shortness of breath
4. Pale skin
5. Decreased urine output
6. Confusion and disorientation
Treatment:
The treatment of low cardiac output depends on the underlying cause. Treatment may include:
1. Medications to increase heart rate and contractility
2. Diuretics to reduce fluid buildup in the body
3. Oxygen therapy to increase oxygenation of tissues
4. Mechanical support devices, such as intra-aortic balloon pumps or ventricular assist devices
5. Surgery to repair or replace damaged heart tissue
6. Lifestyle changes, such as a healthy diet and regular exercise, to improve cardiovascular health.
Prevention:
Preventing low cardiac output involves managing any underlying medical conditions, taking medications as directed, and making lifestyle changes to improve cardiovascular health. This may include:
1. Monitoring and controlling blood pressure
2. Managing diabetes and other chronic conditions
3. Avoiding substances that can damage the heart, such as tobacco and excessive alcohol
4. Exercising regularly
5. Eating a healthy diet that is low in saturated fats and cholesterol
6. Maintaining a healthy weight.
1. Ischemic stroke: This is the most common type of stroke, accounting for about 87% of all strokes. It occurs when a blood vessel in the brain becomes blocked, reducing blood flow to the brain.
2. Hemorrhagic stroke: This type of stroke occurs when a blood vessel in the brain ruptures, causing bleeding in the brain. High blood pressure, aneurysms, and blood vessel malformations can all cause hemorrhagic strokes.
3. Transient ischemic attack (TIA): Also known as a "mini-stroke," a TIA is a temporary interruption of blood flow to the brain that lasts for a short period of time, usually less than 24 hours. TIAs are often a warning sign for a future stroke and should be taken seriously.
Stroke can cause a wide range of symptoms depending on the location and severity of the damage to the brain. Some common symptoms include:
* Weakness or numbness in the face, arm, or leg
* Difficulty speaking or understanding speech
* Sudden vision loss or double vision
* Dizziness, loss of balance, or sudden falls
* Severe headache
* Confusion, disorientation, or difficulty with memory
Stroke is a leading cause of long-term disability and can have a significant impact on the quality of life for survivors. However, with prompt medical treatment and rehabilitation, many people are able to recover some or all of their lost functions and lead active lives.
The medical community has made significant progress in understanding stroke and developing effective treatments. Some of the most important advances include:
* Development of clot-busting drugs and mechanical thrombectomy devices to treat ischemic strokes
* Improved imaging techniques, such as CT and MRI scans, to diagnose stroke and determine its cause
* Advances in surgical techniques for hemorrhagic stroke
* Development of new medications to prevent blood clots and reduce the risk of stroke
Despite these advances, stroke remains a significant public health problem. According to the American Heart Association, stroke is the fifth leading cause of death in the United States and the leading cause of long-term disability. In 2017, there were over 795,000 strokes in the United States alone.
There are several risk factors for stroke that can be controlled or modified. These include:
* High blood pressure
* Diabetes mellitus
* High cholesterol levels
* Smoking
* Obesity
* Lack of physical activity
* Poor diet
In addition to these modifiable risk factors, there are also several non-modifiable risk factors for stroke, such as age (stroke risk increases with age), family history of stroke, and previous stroke or transient ischemic attack (TIA).
The medical community has made significant progress in understanding the causes and risk factors for stroke, as well as developing effective treatments and prevention strategies. However, more research is needed to improve outcomes for stroke survivors and reduce the overall burden of this disease.
There are several types of ischemia, including:
1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.
Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.
Angiotensin II receptor blocker
Fimasartan
Pathophysiology of heart failure
Discovery and development of angiotensin receptor blockers
Valsartan
Hypertension and the brain
List of MeSH codes (D27)
Telmisartan
Angiotensin II receptor type 1
Forasartan
AT1
Antagonism (chemistry)
Corneal neovascularization
Polycystic kidney disease
Alström syndrome
Tachycardia-induced cardiomyopathy
Renin-angiotensin system
Brain natriuretic peptide 32
Arteriosclerosis
AA amyloidosis
Candesartan
Fostamatinib
Type 2 diabetes
Losartan
Magnesium deficiency
Antihypertensive drug
Hyperkalemia
Amiloride
Pemphigoid
Atenolol
COVID-19
Pharmaceutical industry
Diffuse proliferative nephritis
Fenoldopam
Glossary of diabetes
Phosphate nephropathy
Septic shock
Diabetic cardiomyopathy
Vascular dementia
Chronic cough
Complications of hypertension
Hypoglycemia
Sickle cell nephropathy
TRPA1
Spironolactone
Diabetic nephropathy
Anil Pareek
Q-Symbio
Ranitidine
Amlodipine
Gout
Thiazide
Heart failure with preserved ejection fraction
Blood pressure
Diuretic
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Antagonist6
- Furthermore, administering an angiotensin (1-7) antagonist to Opg-KO mice diminished the protective effect of olmesartan against AAA progression. (bvsalud.org)
- We studied the ability of the AT1 receptor antagonist losartan to cure or prevent AD hallmarks in aged (~18 months at endpoint, 3 months treatment) or adult (~12 months at endpoint, 10 months treatment) human amyloid precursor protein (APP) transgenic mice. (nih.gov)
- An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II . (lookformedical.com)
- Chiolero A, Burnier M. Pharmacology of valsartan, an angiotensin II receptor antagonist. (palsforhealth.com)
- Indapamina (diuretic) had a stronger effect than enalapril, and losartan (angiotensin II receptor type 1 (AT1) receptor antagonist) produced better results than atenolol (selective β1 receptor antagonist) with respect to LVH regression. (unesp.br)
- Elesclomol Conversely CI was elevated by Ang II (≥9.6%) CGP42112A (≥14%) and NP-6A4 (≥25%) respectively which impact was blocked by AT2R antagonist PD123319 however not by AT1R antagonist losartan. (mdm2-inhibitors.com)
Losartan6
- Losartan attenuated astrogliosis, normalized AT1 and AT4 receptor levels, but failed to rescue the cholinergic deficit and the Aβ pathology. (nih.gov)
- We conclude that losartan exerts potent preventive and restorative effects on AD hallmarks, possibly by mitigating AT1-initiated oxidative stress and normalizing memory-related AT4 receptors. (nih.gov)
- Concurrently, mice were intracerebroventricularly infused with the AT1R blocker losartan, angiotensin-converting-enzyme inhibitor captopril, or artificial cerebrospinal fluid for 3 wk. (nih.gov)
- Intracerebroventricular infusion of losartan or captopril attenuated DOCA-salt-induced PRR mRNA elevation in the paraventricular nucleus of the hypothalamus, suggesting a role for ANG II/AT1R signaling in regulating PRR expression during DOCA-salt hypertension. (nih.gov)
- Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN . (nih.gov)
- To be able to determine differences in cardiovascular cell response during nutritional stress to different cardiovascular defensive medications we investigated cell responses of serum starved mouse cardiomyocyte HL-1 cells and principal cultures of individual coronary artery vascular even muscles (hCAVSMCs) to treatment with β-blockers (atenolol metoprolol carvedilol nebivolol 3 each) Elesclomol AT1R blocker losartan (1μM) and AT2R agonists (CGP42112A and novel agonist NP-6A4 300 each). (mdm2-inhibitors.com)
ARBs9
- Background Angiotensin II type 1 receptor blockers (ARBs) have been shown to limit the growth of abdominal aortic aneurysm (AAA), but their efficacy is controversial. (bvsalud.org)
- In cultured vascular smooth muscle cells , tumor necrosis factor -related apoptosis -inducing ligand -induced c-Jun N-terminal kinase phosphorylation and matrix metalloproteinase 9 expression were inhibited by angiotensin (1-7), the circulating levels of which are increased by ARBs. (bvsalud.org)
- Conclusions Olmesartan prevented AAA progression in Opg-KO mice by upregulating angiotensin (1-7), suggesting that angiotensin (1-7) may be a key factor that mediates the protective effect of ARBs. (bvsalud.org)
- One potentially lethal example is that patients who take renin-angiotensin system (RAS) blockers, particularly angiotensin II type 1 receptor blockers (ARBs), may be more susceptible to the virus. (medicalxpress.com)
- In the article "Renin-angiotensin system (RAS) blockers and the COVID-19 pandemic: at present there is no evidence to abandon RAS blockers," Dr. Epstein and coauthors Jan Danser, Ph.D., of Erasmus Medical Center in Rotterdam, and Daniel Batlle, M.D., at Northwestern University, carefully reviewed the available data to determine whether ARBs pose any significant risk. (medicalxpress.com)
- Though some studies have shown ARBs increase ACE 2 activity in animal models, it must be emphasized that the results have been inconsistent. (medicalxpress.com)
- Should angiotensin receptor blockers (ARBs) be taken with or without food? (palsforhealth.com)
- Angiotensin receptor blockers (ARBs) do not have to be taken with food. (palsforhealth.com)
- Angiotensin II (Ang II) acting through the AT1R is an important contributor to vasoconstriction and promotes cardiac hypertrophy fibrosis and heart disease [22 23 Moreover AT1R activation induces adult cardiomyocyte cell death [24 25 AT1R blockers (ARBs) are another group of widely used medicines to treat individuals with hypertension atherosclerosis coronary heart disease restenosis and heart failure. (mdm2-inhibitors.com)
Hypertension15
- This study is a test of the safety and effectiveness of two drugs, one for diabetes and one for hypertension, in keeping patients with high lab values of glucose from progressing to frank diabetes and developing cardiovascular complications. (clinicaltrials.gov)
- 1 Oklahoma Cardiovascular and Hypertension Center and the University of Oklahoma College of Medicine, Oklahoma City, OK, USA. (nih.gov)
- The median duration (IQ) of hypertension diabetics was 4 (1-10) years. (hindawi.com)
- The World Health Organization projected that 300 million people will suffer from diabetes and 1.5 billion [ 1 ] from hypertension by 2025 [ 2 ]. (hindawi.com)
- The incidence of hypertension in patients with T2DM is approximately two-fold higher than in age-matched subjects without the disease [ 4 ]. (hindawi.com)
- A.H. Jan Danser et al, Renin-Angiotensin System Blockers and the COVID-19 Pandemic, Hypertension (2020). (medicalxpress.com)
- The leading cause of end-stage renal disease (ESRD) (i.e., kidney failure requiring dialysis or transplantation) in the United States is diabetes, followed by hypertension and glomerulonephritis ( 1 ). (cdc.gov)
- During 1994--2004, ESRD incidence with hypertension listed as the primary diagnosis was at least three times higher among blacks than among the other three racial populations ( Figure 2 ). (cdc.gov)
- As many as two-thirds of patients Treatment: blood pressure goals and with type 2 diabetes have hypertension. (who.int)
- To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II , patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS . (lookformedical.com)
- An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE . (lookformedical.com)
- Clinical pharmacokinetics of angiotensin II (AT1) receptor blockers in hypertension. (palsforhealth.com)
- Candesartan is used to treat high blood pressure (hypertension) in adults and children who are at least 1 year old. (cigna.com)
- Aim The aim of this study is to discuss the reliable scientific evidence of an interactive link between hypertension and hypercholesterolemia considering the metabolic pathways and the pathogenetic mechanisms connecting the two risk factors. (unibo.it)
- Although the mechanisms of interaction between these two risk factors have not been completely elucidated thus far, there is rapidly growing evidence that the involvement of the renin-angiotensin system (RAS) can be considered as the common link between hypertension and hypercholesterolemia. (unibo.it)
Antagonists1
- Michel MC, Foster C, Brunner HR, Liu L. A systematic comparison of the properties of clinically used angiotensin II type 1 receptor antagonists. (palsforhealth.com)
Converting Enzyme7
- They note the concern originated from reports that the angiotensin-converting enzyme 2 (ACE 2) protein receptor may enable viral entry into cells. (medicalxpress.com)
- It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. (lookformedical.com)
- It is converted to angiotensin II , a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. (lookformedical.com)
- Renin , an enzyme produced in the kidney , acts on angiotensinogen , an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I . Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II , an extremely powerful vasoconstrictor. (lookformedical.com)
- Angiotensin-converting enzyme also breaks down BRADYKININ , a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM. (lookformedical.com)
- Enalapril (angiotensin-converting enzyme inhibitor) and verapamil (Ca++ channel blocker) caused hypertrophy to regress in LVH rats. (unesp.br)
- Several interventions, such as tight glycemic control and antihypertensive therapy, especially angiotensin converting enzyme inhibitors (ACEIs) and angiotensinII receptor blockers, have been shown to slow the progression of established disease. (nephronpower.com)
Telmisartan1
- The investigator will evaluate if telmisartan is able to influence the renin-angiotensin system in the brain and produce favorable effects on brain blood flow and enzymes that cause the brain plaques in Alzheimer's disease.The investigator will assess the mechanism by which telmisartan modifies the brain renin angiotensin system, cerebrospinal fluid amyloid-β, cerebral blood flow (CBF) and inflammatory markers in hypertensive African Americans. (clinicaltrials.gov)
Hypertensive3
- Review Article hypertensive drugs.22 Although lifestyle modifications Calcium channel blockers are beneficial, consistency is often difficult and only a Although controversy exists on the use of calcium channel few patients are able to achieve blood pressure control blockers (CCBs), particularly dihydropyridines, in pa- with these interventions. (who.int)
- Study on pleiotropic effects of angiotensin II- receptor blockers (ARB) in hypertensive obese patients. (go.jp)
- Anti-hypertensive medicines such as β-adrenergic receptor blockers (β-blockers) and inhibitors of angiotensin II type 1 receptor (AT1R) are reported to exert cardioprotective effects by reducing cardiomyocyte death [7-11]. (mdm2-inhibitors.com)
Pharmacology1
- 1 Institute of Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, Lübeck, Germany. (nih.gov)
20232
Renin10
- Angiotensin II regulates brain (pro)renin receptor expression through activation of cAMP response element-binding protein. (nih.gov)
- Blood pressure medications known as angiotensin-receptor blockers have been associated with reduced risk of Alzheimer's in Caucasians because they act on the renin-angiotensin system (RAS), a key regulator of blood pressure in the body and the brain. (clinicaltrials.gov)
- The cerebrospinal fluid renin-angiotensin system (RAS) will be assessed by measuring levels of angiotensin metabolites sample 1ml of cerebrospinal fluid (CSF). (clinicaltrials.gov)
- They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system . (lookformedical.com)
- Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin. (lookformedical.com)
- A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN , leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM . (lookformedical.com)
- Renin-Angiotensin System Inhibition, Worsening Renal Function, and Outcome in Heart Failure Patients With Reduced and Preserved Ejection Fraction: A Meta-Analysis of Published Study Data. (nih.gov)
- Beldhuis IE, Streng KW, Ter Maaten JM, Voors AA, van der Meer P, Rossignol P, McMurray JJ, Damman K. Renin-Angiotensin System Inhibition, Worsening Renal Function, and Outcome in Heart Failure Patients With Reduced and Preserved Ejection Fraction: A Meta-Analysis of Published Study Data. (nih.gov)
- BACKGROUND: Renin-angiotensin aldosterone system (RAAS) inhibitors significantly improve outcome in heart failure (HF) patients with reduced ejection fraction (HFREF), irrespective of the occurrence of worsening renal function (WRF). (nih.gov)
- Drugs that act directly on the renin-angiotensin system can cause injury and death to the developing fetus. (nih.gov)
Antihypertensive2
- To evaluate prescribing pattern of antihypertensive in T2DM (type 2 diabetes) patients and compare with existing recent guidelines. (hindawi.com)
- Utilization of 5 different antihypertensive drug classes was compared for all patients receiving 1, 2, 3, 4, or more drugs. (hindawi.com)
Candesartan3
- 11. The angiotensin II type 1 receptor blocker candesartan suppresses proliferation and fibrosis in gastric cancer. (nih.gov)
- Candesartan is an angiotensin II receptor blocker (sometimes called an ARB). (cigna.com)
- Candesartan is also used in adults to treat certain types of heart failure and lower your risk of death or needing to be hospitalized for heart damage. (cigna.com)
Upregulation3
- Angiotensin II Type 1 Receptor Blocker Prevents Abdominal Aortic Aneurysm Progression in Osteoprotegerin-Deficient Mice via Upregulation of Angiotensin (1-7). (bvsalud.org)
- ANG II also induced PRR upregulation in primary cultured neurons. (nih.gov)
- In particular, hypercholesterolemia seems to promote the upregulation of type 1 angiotensin II (AT1) receptor genes because of an increase in the stability of mRNA followed by structural overexpression of vascular AT1 receptors for angiotensin II. (unibo.it)
Valsartan3
- For the first 2 weeks of treatment, patients took the combination of nateglinide 30 mg (3 times daily, ante cibum [ac] before meals) and valsartan 80 mg (once daily [od] in the morning). (clinicaltrials.gov)
- After 2 weeks, patients were up-titrated to nateglinide 60 mg ac and valsartan 160 mg od. (clinicaltrials.gov)
- For the first 2 weeks of treatment, patients took valsartan 80 mg capsules (once daily [od] in the morning). (clinicaltrials.gov)
Agonist2
- As an agonist of Mas receptors, angiotensin-(1-7) has beneficial cardiovascular and metabolic effects. (nih.gov)
- Liraglutide, a glucagonlike peptide-1 (GLP-1) agonist, is the first noninsulin drug approved to treat type 2 diabetes in pediatric patients since metformin was approved for pediatric use in 2000. (medscape.com)
Enalapril1
- The effects of enalapril and nifedipine (Ca++ channel blocker) were similar. (unesp.br)
Drugs2
- Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR. (lookformedical.com)
- Of current drugs, Cherezov says, "It's like using a 2-by-4 to kill a fly. (nih.gov)
Amino acids2
- AN - not for activation of enzymes, receptors, cells, etc. by amino acids: index ENZYME ACTIVATION or specific term with /metab HN - 2005 MH - Anabaena cylindrica UI - D046868 MN - B3.280.100.150 MN - B3.440.475.100.100.150 MS - A species in the genus ANABAENA whose trichomes are composed of cylindrical cells. (nih.gov)
- Mutating these parts of the protein revealed which specific amino acids in the receptor were critical for binding. (nih.gov)
AT1R5
- To address whether ANG II type 1 receptor (AT1R) signaling is involved in this regulation, we implanted a DOCA pellet and supplied 0.9% saline as the drinking solution to C57BL/6J mice. (nih.gov)
- To test which ANG II/AT1R downstream transcription factors were involved in PRR regulation, we treated Neuro-2A cells with ANG II with or without CREB (cAMP response element-binding protein) or AP-1 (activator protein-1) inhibitors, or CREB siRNA. (nih.gov)
- One of the ways the human body regulates blood pressure is through a molecule called the angiotensin II type 1 receptor (AT1R). (nih.gov)
- The researchers were able to determine the structure of AT1R when bound to an angiotensin receptor blocker called ZD7155. (nih.gov)
- Unlike AT1R activation of Ang II type 2 receptor (AT2R) causes vasodilation and enhances cardiac restoration after MI [27 28 We have demonstrated that AT2R activation can inhibit AT1R-mediated inositol 1 4 5 generation and that the 3rd intracellular loop of AT2R is required for this effect [29]. (mdm2-inhibitors.com)
Cardiovascular6
- 2 DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Lübeck, Germany. (nih.gov)
- An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY , the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. (lookformedical.com)
- Myeloid Cell Leukemia 1 (MCL-1) is definitely a protein critical for cardiovascular cell survival and implicated in cell adhesion. (mdm2-inhibitors.com)
- These data display for the first time that activation of the AT2R-MCL-1 axis by NP-6A4 in nutrient-stressed mouse and human being cardiovascular cells (mouse HL-1 cells and main ethnicities of hCAVSMCs) might underlie improved survival of cells treated by NP-6A4 compared to additional medicines tested with this study. (mdm2-inhibitors.com)
- Introduction Cardiovascular diseases particularly ischemic heart disease are the number one cause of death world-wide despite commendable improvements in acute care and pharmacotherapy [1-4]. (mdm2-inhibitors.com)
- However further studies are needed to fully understand the protective effects of Neb compared to additional β-blockers on cardiovascular cells subjected to nutrient stress. (mdm2-inhibitors.com)
VASODILATION1
- Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR. (lookformedical.com)
Bind5
- Angiotensin II (AngII) receptor blockers that bind selectively AngII type 1 (AT1) receptors may protect from Alzheimer's disease (AD). (nih.gov)
- Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells. (lookformedical.com)
- They specifically identified the components that make up the receptor's binding pocket, where the blockers bind to cause their effects. (nih.gov)
- The researchers used this information to develop simulations of what happens in the binding pocket when other angiotensin receptor blockers bind to it. (nih.gov)
- To do so, you need to understand exactly how and where drug-like molecules bind to the receptor and what conformational changes they produce. (nih.gov)
Protein2
- We measured protein levels of oxidative stress enzymes (superoxide dismutases SOD1, SOD2 and NADPH oxidase subunit p67phox), and quantified soluble and deposited amyloid-β (Aβ) peptide, glial fibrillary acidic protein (GFAP), AngII receptors AT1 and AT2, angiotensin IV receptor AT4, and cortical cholinergic innervation. (nih.gov)
- Membrane-bound form of monocyte chemoattractant protein-1 enhances antitumor effects of suicide gene therapy in a model of hepatocellular carcinoma. (kanazawa-u.ac.jp)
Rats2
Diabetes11
- In January 2013, the American Academy of Pediatrics (AAP) issued clinical practice guidelines on the management of type 2 diabetes in children and adolescents. (medscape.com)
- The guidelines recommend insulin treatment in all patients who present with ketosis or extremely high blood glucose levels because it may not be clear initially whether these patients have type 2 or type 1 diabetes. (medscape.com)
- Once a diagnosis of type 2 diabetes is confirmed, lifestyle modification and metformin treatment should be initiated. (medscape.com)
- Unless an acute complication (eg, recurrent hypoglycemia, persistent ketosis, hyperglycemic hyperosmolar state) occurs or there is poor patient compliance with treatment, type 2 diabetes is usually managed in an outpatient setting. (medscape.com)
- A study by Loimaala et al study showed that long-term endurance and strength training resulted in improved metabolic control of type 2 diabetes compared with standard treatment. (medscape.com)
- Because type 2 diabetes in children and adolescents is strongly associated with obesity and sedentary lifestyle, any intervention designed to increase physical activity and improve dietary habits should be encouraged. (medscape.com)
- In June 2019, the US Food and Drug Administration (FDA) approved liraglutide for children aged 10 years or older with type 2 diabetes mellitus. (medscape.com)
- During 1994--2004, age-adjusted ESRD incidence with diabetes listed as the primary diagnosis was higher among blacks and AI/ANs than among whites and A/PIs ( Figure 1 ). (cdc.gov)
- with type 2 diabetes. (who.int)
- Traditional contraindications for β-blockers include peripheral vascular diseases diabetes mellitus chronic obstructive pulmonary disease (COPD) and asthma [12-14]. (mdm2-inhibitors.com)
- Nevertheless,DN remains a major long-term complication of both types 1 and 2 diabetes. (nephronpower.com)
Vascular1
- Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure . (lookformedical.com)
Progression4
- Olmesartan prevented AAA progression in Opg-KO mice , including excessive aortic dilatation and collapse of tunica media , but not in wild-type mice . (bvsalud.org)
- 1. Importance of human peritoneal mesothelial cells in the progression, fibrosis, and control of gastric cancer: inhibition of growth and fibrosis by tranilast. (nih.gov)
- 2. The role of human peritoneal mesothelial cells in the fibrosis and progression of gastric cancer. (nih.gov)
- We sought to (1) establish and implement the infrastructure for longitudinal, virtual follow-up of clinical trial participants, (2) compare changes in smartphone-based assessments, online patient-reported outcomes, and remote expert assessments, and (3) explore novel digital markers of Parkinson's disease disability and progression. (nutrition-evidence.com)
Effects1
- Angiotensin receptor blockers are used to treat high blood pressure, but can have other effects. (nih.gov)
Kidney2
- Continued interventions, such as those addressing blood-glucose and blood-pressure control ( 2,3 ), are needed to reduce the prevalence of these risk factors for kidney failure ( 4 ) and to improve care among persons with these conditions. (cdc.gov)
- In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney . (lookformedical.com)
Activates1
- When the hormone angiotensin II binds to this receptor, it activates a pathway involving signaling molecules called G-proteins that constricts blood vessels and raises blood pressure. (nih.gov)
Patients4
- Patients not tolerating the higher dose (Level 2) were down-titrated to receive Level 1. (clinicaltrials.gov)
- Patients not tolerating the lower dose (Level 1) had a treatment interruption. (clinicaltrials.gov)
- USRDS collects demographic and clinical data, including the date patients were first treated and the primary diagnosis, on all ESRD patients and includes data for approximately 93% of persons with ESRD in the United States ( 1 ). (cdc.gov)
- A total of 8 studies (6 HFREF and 2 HFPEF, including 28 961 patients) were included in our analysis. (nih.gov)
Activation1
- Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention. (lookformedical.com)
Agonists1
- Angiotensin-(1-7)-like agonists may be drug candidates for treating obesity. (nih.gov)
Treatment3
- Following each change in dose level or re-initiation of treatment, tolerability was assessed after 2 weeks of exposure. (clinicaltrials.gov)
- Through the ESRD entitlement program, Medicare reimburses most of the total cost of ESRD treatment in the United States ( 1 ). (cdc.gov)
- The treatment of both risk factors greatly improves individual risk profile, especially when statins and RAS blockers are used together. (unibo.it)
Blood pressure3
- ACE 1 helps to regulate blood pressure by converting angiotensin I to angiotensin II. (clinicaltrials.gov)
- A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A . It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II , a vasoconstrictor and important regulator of arterial blood pressure . (lookformedical.com)
- About 1 in 3 American adults has high blood pressure. (nih.gov)
Mice2
- Methods and Results Olmesartan, an ARB, was administered to wild-type and osteoprotegerin -knockout (Opg-KO) mice starting 2 weeks before direct application of CaCl2 to aortas to induce AAA. (bvsalud.org)
- The protective effect of olmesartan against AAA in wild-type and Opg-KO mice was compared at 6 weeks after AAA induction. (bvsalud.org)
Responses1
- We tested learning and memory with the Morris water maze, and evaluated neurometabolic and neurovascular coupling using [18F]fluoro-2-deoxy-D-glucose-PET and laser Doppler flowmetry responses to whisker stimulation. (nih.gov)
Significantly1
- β-blockers significantly suppressed and NP-6A4 improved MCL-1 manifestation in HL-1 and hCAVSMCs as determined by immunofluorescence. (mdm2-inhibitors.com)
Levels2
- CREB and AP-1 inhibitors, as well as CREB knockdown abolished ANG II-induced increases in PRR levels. (nih.gov)
- An angiotensin receptor subtype that is expressed at high levels in fetal tissues. (lookformedical.com)
Intake1
- Angiotensin-(1-7) regulated food intake and body weight and contributed to the weight loss after AT1 receptor blockade. (nih.gov)
Phase1
- METHODS Participants from two recently completed phase III clinical trials of inosine and isradipine enrolled in Assessing Tele-Health Outcomes in Multiyear Extensions of Parkinson's Disease trials (AT-HOME PD), a two-year virtual cohort study. (nutrition-evidence.com)