BLUE PRINT 3

Anti-diuretic hormone (ADH)

Another hormone acting on the kidney is the Antidiuretic Hormone (ADH) -- is also known as arginine vasopressin. 1. It's synthesized in the hypothalamus 2. Then, migrates to the posterior pituitary gland for storage. -The primary function of ADH is to regulate the amount of water reabsorbed by the kidneys. It does this by acting on the nephrons, the functional units of the kidneys, to make them more permeable to water. This increased water reabsorption reduces the amount of water excreted in urine, resulting in more concentrated urine. In essence, ADH helps the body conserve water when it is needed to maintain proper fluid balance -ADH has two effects... 4. It has an effect on blood vessels causing vasoconstriction increasing BP 5. It has an effect on the kidney by increasing the permeability of the distal tubule and collecting duct membrane to water, so.... It increases reabsorption of water increasing blood volume •Because of increased water reabsorption from the filtrate the urine becomes more concentrated •And there's a decrease in the amount of urine produced

Pre-renal failure

Pre-renal failure implies a state of relative hypoperfusion to an otherwise normal kidney...hint! hint!..important to know this definition...you have a normal kidney, it's just not being perfused well. -The glomeruli are unable to filter waste from the blood because of decreased renal blood flow. •Functionally and structurally the renal tubules are intact •So, the kidneys retain more Na+ and water attempting to correct what they perceive to be a volume deficit so that by increasing intravascular volume - blood pressure is increased - renal blood flow increases - and GFR then improves

Glomerular filtration rate

The rate at which fluid filters from the blood into the Bowman's capsule is known as the glomerular filtration rate (GFR)...hint! hint! important concept to remember because anything that affects cardiac output can affect GFR

Hint hint about GFR

The rate at which fluid filters from the blood into the Bowman's capsule is known as the glomerular filtration rate (GFR)...hint! hint! important concept to remember because anything that affects cardiac output can affect GFR

Unstable angina

a combination of classic and variant angina • it is seen in individuals with worsening CAD • typically the atherosclerotic plaque has become complicated • episodes of unstable angina increase in frequency • signals infarct is near

Acute tubular necrosis

•Occurs secondary to ischemic or toxic injury to renal tubules. •Occurs when mean arterial pressure is decreased. The afferent and efferent arterioles lose their autoregulatory process with hypoperfusion •Sympathetic stimulation (increased catecholamine release) and angiotensin II cause severe vasoconstriction •Hypoxia also leads to cellular damage

Acute renal failure

•loss of water & electrolyte homeostasis •secondary to an abrupt & severe decrease in GFR • and is associated with a decrease in UOP, progressive increase in BUN, and increase Cr

Pre-renal azotemia

This type of azotemia occurs when the problem is located upstream of the kidneys, before the blood reaches the renal (kidney) arteries. Common causes include reduced blood flow to the kidneys due to conditions like dehydration, heart failure, or severe bleeding. In these cases, the kidneys are not receiving enough blood to effectively filter waste products.

Acute glomerulonephritis

Acute glomerulonephritis & pyelonephritis : streptococcus disease,syphilis, toxoplasmosis, viral, hepatitis B, mononucleosis, measles & mumps. -Acute glomerulonephritis is a medical condition characterized by inflammation of the glomeruli, which are tiny filters in the kidneys responsible for removing waste products and excess fluids from the blood. This inflammation can affect the kidney's ability to function properly and can lead to a range of symptoms and complications.

Glomerulonephritis

Acute poststreptococcal glomerulonephritis -Occurs after throat/skin infection from group A strep, follows within 7-12 days post infection -Onset of hematuria, HTN, edema, renal insufficiency -Antigen-antibody complexes and complements are deposited into the glomerulus -immune complexes initiate inflammation and glomular injury -95% recoverable for children, 60% for adults

Hypertrophic cardiomyopathy

*** circle, star and underline*** important finding in this myopathy that helps distinguish it (from other myopathies) is that the there are myofibril disarray (which means that the muscle fibers of the heart are not in the typical lattice pattern) this produce uncoordinated contraction & relaxation and can lead to sudden death*** -***36% of young athletes who die suddenly on autopsy were found to have idiopathic hypertrophic cardiomyopathy. While the cause is unknown it is thought to be familial. And, if one sibling in the family has cardiomyopathy - all the siblings should be evaluated for cardiomyopathy

primary mechanism in atherosclerosis developmen

*inflammation with oxidative stress & activation of macrophages

Left heart failure

- Failure of left heart to move blood from the pulmonary circulation into the systemic circulation • Leading to a decrease in cardiac output • Increase in left atrial & left ventricular end-diastolic pressures • Congestion in the pulmonary circulation -•Associated conditions: •Acute myocardial infarction •Stenosis or regurgitation of mitral/aortic valves •Rapid infusion of IVF or blood -Forward effects of left heart failure •Decreased systemic blood pressure •Fatigue •Increased heart rate •Decreased urine output -Backward effects of left heart failure •Increased pulmonary congestion (especially when lying down) •Dyspnea (difficulty breathing) •Right heart failure if condition worsens

Aldosterone (2)

-Aldosterone is a steroid hormone produced by the adrenal glands, which are small glands located on top of each kidney. It plays a crucial role in regulating the body's electrolyte balance, blood pressure, and fluid balance -Renin-Angiotensin-Aldosterone System (RAAS) regulates the ECF volume by regulating sodium content. Stimulation of this system leads to: 1. Systemic vasoconstriction 2. Sodium retention in kidneys (along with Na+ goes H2O) 3. Expansion of ECF volume It does this through the stimulation of renin Renin is an enzyme produced by the juxtaglomerular cells of the nephrons. Which are cells are located in the walls of the afferent arteriole. They act as baroreceptors (responding to renal blood flow)

Systolic heart failure

-Decrease in myocardial contractility and EF under 40%. Severe is under 10%. -W/ decreased EF, there is increase in end-diastolic volume (preload), ventricular dilation, ventricular wall tension, and a rise in ventricular end-diastolic pressure. -Increased volume, added to normal venous return leads to increase in ventricular preload. -Increased preload leads to accumulation of blood in atria and the venous system causing pulmonary or peripheral edema. -Systolic dysfunction results from conditions that impair contractile performance of the heart, produce a volume overload, or generate pressure overload of the heart. -can be estimated by measuring CO and EF

Secondary Hypertension

-Elevated BP (180/110) d/t identifiable underlying condition -Features: Organ damage or malignant HTN -Can return to normal BP if underyling is corrected -Underlying diseases: Renal (renalvascular, glomerulonephritis, PKD, diabetic nephropathy) -Endocrine (Cushings, hyperthyroidism, pheochrocytoma) -Increase intervascular volume, medications

Syndrome of inappropriate antidiuretic hormone (SIADH)

-Increased ADH release, increased reabsoprtion water in CT -UOP decrease (as the kidney is reabsorbing more water) •Concentrated urine (increased sp gravity...can be over 1.020) •Patients appear edematous •Decreased serum sodium •Increased weight gain •Can be seen in patients with CNS disease, also there is increased ADH release when patients are in pain, have surgery, asphyxia, pneumothorax

Capillary/Interstitial hydrostatic pressure

-Increased capillary hydrostatic pressure causes edema -(think increased volume or increased pressure) in which the increased pressure forces excessive amounts of fluid out of the capillaries into the tissues. Just remember it's the force that "pushes" fluid out. -An example would be pulmonary edema in which excessive pressure in the vascular bed (often due to increased volume -hypervolemia) forces fluid from the pulmonary capillaries into the alveoli which then interferes with respiratory function.

Fusiform abdominal aortic aneurysm

-Involves entire circumference of vessel w/ gradual and progressive vessel dilation. -May involve ascending and transverse portions of thoracic aorta or may extend to large portions of abdominal aorta -Fusiform aneurysms are typically elongated and spindle-shaped. They involve the entire circumference of the aorta and cause it to dilate uniformly. -often associated with atherosclerosis, abdominal and back pain. CT scans/mri

Myocardial Infarction (2)

-Irreversible ischemia, if becomes occluded for more than 20 mins- infarct -it is the death of myocardial cells following prolonged deprivation • it is the culminating lethal response to unrelieved myocardial ischemia -Structural & functional changes •Despite almost immediate onset of EKG changes, gross tissue changes in the area of infarction may not be apparent for several hours • The infarcted myocardium is surrounded by a zone of hypoxic injury which may progress to: •Necrosis •Undergo remodeling •or, return to normal • Tissue surrounding the area of infarction also undergoes changes known as: • Myocardial stunning temporary loss of contractile function • Can last for hours to days after perfusion has been restored • Hibernating issue undergoes metabolic adaptation to preserve the cell until perfusion is restored • Remodeling (under influence of angiotension II) causes hypertrophy and loss of contractile function in areas distant from the site of infarction •Repair (usually starts within 10-14 days after episode) consists of degradation of damaged cells, proliferation of fibroblasts formation of scar tissue • Scar tissue is strong but unable to contract & relax like healthy myocardial tissue • By six weeks the necrotic area is completely replaced by scar tissue

Left ventricular failure

-LV Diastolic dysfunction, normal LV systolic fx: -Prevalence increases w/ age and higher in men than woman. -During exercise stroke volume does not increase normally, even w/ increased LV filling pressure -, myocardial hypertrophy, ischemia, or fibrosis causes slow or incomplete LV filling at normal left atrial pressures. Left atrial pressure rises to increase LV filling, resulting in pulmonary and systemic venous congestion. The development of AF (the prevalence of which increases with age) may also cause a decrease in cardiac output and the development of pulmonary and systemic venous congestion, because of the loss of left atrial contribution to LV late diastolic filling and reduced diastolic filling time due to a rapid ventricular rate.-LV systolic dysfunction: LVEF < 50%. -Myocardial fiber shortening is reduced. -Stroke volume decreased. -LV is dilated. -Pt symptomatic. -Symptoms: Dyspnea, paroxysmal nocturnal dyspnea, dyspnea at rest, pulmonary edema/ congestion. -Decreased cardiac output may cause weakness, feeling of heaviness, nocturia, oliguria, confusion, insomnia, HA, anxiety, memory impairment, Epigastric or RUQ ache, fullness after eating, N/V

Renal Carcinoma (Hypernephroma)

-Malignant tumor that accounts for 90% of all primary renal CA's -Imaging, CT scanning, ultrasound, helps w early diagnosis -Silent disorder, hematuria, flank pain, palpable flank mass

Primary Hypertension

-Primary: specific cause not yet identified though thought to be combination of genetics and environment. Also, known as essential or idiopathic hypertension affects 90-95% of individuals with hypertension. The above is a path map showing the contribution of increased PVR and increased blood volume leading to sustained hypertension

Chronic pyelonephritis

-Pyelonephritis refers to infection of kidney parenchyma and renal pelvis -Chronic: scarring and deformation of the renal calyces ad pelvis -involve a bacterial infection superimposed on obstructive abnormalities or vesicoureteral reflux -Recurrent UTI's, loss of tubular fx, polyuria, nocturia, mild proteinuria -Signifigant cause of renal failure

Diastolic ventricular dysfunction

-Relaxation is abnormal. Abnormal ventricle filling hurts CO, esp during exercise. increased with age and in woman. -Conditions that cause DV dysfunction are those that impede expansion of ventricle (pericardial effusion, constrictive pericarditis), those that increase wall thickness and reduce chamber size, and those that delay relaxation during diastole -Increased HR

Osteodystrophy

-Renal Osteodystrophy: Renal osteodystrophy is the term used to describe bone abnormalities that develop as a result of CKD and the associated mineral and hormonal imbalances. It encompasses various bone disorders -Osteodystrophy in CKD can lead to a range of symptoms, including bone pain, muscle weakness, fractures, and deformities.

Restrictive cardiomyopathy

-Restrictive cardiomyopathy (least common type of myopathy seen in western countries). In this process the ventricular filling is restricted because of excessive rigidity (stiffness) of the walls . A common cause is endothelial infiltration with amyloid or glycogen storage disease. -Symptoms similar to pericarditis and all signs of heart failure (particularly right heart failure) -Amyloidosis is a common cause of restrictive myocarditis - these are deposits of abnormal protein (amyloid) in the heart. This abnormal protein slowly replace normal heart muscle eventually leading to heart failure. Once the diagnosis has been made - the lifespan of the individual (without transplant) is less than one year.

Silent Ischemia

-Silent myocardial Ischemia: Absence of angial pain, caused by impaired blood flow. -Affects ppl who are asymptomatic w/o evidence of CAD, ppl who have had a myocardial infarct and continue to have episodes of silent ischemia, and ppl w/ angina who also have episodes of silent ischemia.

Stages of renal failure (CKD)

-Stage 1: Kidney damage w/ normal or elevated GFR (>90) -Stage 2: Kidney damage w/ mild decrease GFR (60-89) Stage one to two is that of diminished renal reserve GFR drops to ~60% of normal •BUN, CR still normal, no symptoms •May have only one kidney or be functioning on one kidney -Stage 3: Moderate decrease GFR (30-59) -Stage 4: Severe decrease GFR (15-29) Stage three to four is that of renal insufficiency GFR is 50 to 20% normal •Azotemia •Anemia •Hypertension begins to appear (usually late 2 or 3) -Stage 5: Kidney failure GFR (<15) Diaylsis Stage (late) four to five is renal failure GRF 20 to 5% normal •Kidneys can't regulate volume and solute composition •Electrolytes abnormal •Edema develops -Metabolic acidosis -ESRD GFR is less than 5% •Dialysis or transplantation is necessary for survival •Reduction in renal capillaries •Scarring in glomeruli •Atrophy & fibrosis in tubules

Intrinsic renal failure

-Uncorrected prerenal failure can progress to frank renal damage and can lead to intrinsic failure! -loss of renal function due to structural damage to the glomeruli and/or tubules •Tubule epithelial cells separate from the basement membrane and slough into the lumen •Damage can occur anywhere along the nephrons -Conditions resulting in Intrinsic failure are: •Ischemia associated with prerenal failure •Toxic insult to tubular structures •Acute glomerulonephritis & pyelonephritis -Congenital renal abnormalities can cause intrinsic failure Cystic dysplasia of kidney **The most common cause of intrinsic failure is Acute Tubular Necrosis (ATN) ...hint! hint! remember this

Cardiac tamponade

-acute compression of the heart caused by fluid accumulation in the pericardial cavity -Pericardial effusion can lead to cardiac tamponade, the compression of the heart caused by the accumulation of fluid or pus, or blood in the pericardial sac -Results in increased intracardiac pressure, limitation of ventricular diastolic filling, and reductions in stroke volume and CO. Elevation in CVP, JVD, fall in systolic bp, narrowed pulse pressure, muffled heart sounds -LV is compressed by the interventricular septum and pericardium, which decreased LV filling and LV SV. -Echocardiogram -NSAIDS, colchicine, or corticosteroids may minimize fluid. Pericardiocentesis (emergency)

Factors affecting cardiac output/force of contraction

-age and gender but in general ranges from 4.2 to 8 Liters. The heart's ability to increase its output according to body's needs depends on stroke volume (the amount of blood ejected with each beat). •Preload: or, filling of the ventricles (ie end-diastolic volume (EDV) •Afterload or, resistance to ejection of blood from the heart •Contractility determined by the interaction of the actin & myosin filaments of cardiac muscles -

Left ventricular function

-chamber of the heart responsible for pumping oxygenated blood to the body's various tissues and organs -Ejection Fraction (EF): Ejection fraction is a crucial measure of left ventricular function. It represents the percentage of blood that the left ventricle pumps out with each contraction. A normal ejection fraction typically falls in the range of 50% to 70%. An ejection fraction below 50% may indicate reduced left ventricular function. -Contractility: The left ventricle should contract forcefully and efficiently during each heartbeat, allowing it to eject blood into the aorta and subsequently to the rest of the body. Normal left ventricular contractility ensures an adequate supply of oxygenated blood to meet the body's demands. -Relaxation: After each contraction, the left ventricle should relax adequately to allow for the filling of blood from the left atrium. Normal relaxation is essential for maintaining adequate cardiac output and preventing blood from backing up into the lungs. -Wall Thickness: The walls of the left ventricle should have a certain thickness. Hypertrophy or thickening of the left ventricular walls can be seen in conditions like hypertension or aortic stenosis. -Valve Function: The normal function of the aortic and mitral valves is crucial for maintaining proper left ventricular function. These valves ensure that blood flows forward and does not leak back into the atria during ventricular contraction. Symptoms: Normal left ventricular function is typically associated with the absence of symptoms like shortness of breath, chest pain, or fatigue, which might indicate impaired heart function. -Exercise Tolerance: Individuals with normal left ventricular function should have good exercise tolerance, meaning they can engage in physical activities without experiencing excessive fatigue or symptoms related to poor cardiac function.

Dilated cardiomyopathy

-dysfunctional heart muscle because of an enlarged heart -• The dilated heart muscle can cause impaired pumping of one or both ventricles • As the heart enlarges the walls of the ventricle thin • Can see micro-thrombi develop within the heart (as the heart can't eject the blood out wellit "pools" leading clots to develop •The valves (tricuspid and mitral) are often normal but can develop incompetence over time as the ventricle dilates and stretches -Manifestations •Heart failure usually initial finding •Profound dyspnea on exertion (d/t decreased cardiac output and development of pulmonary edema) •Sinus tachycardia, atrial fib, & ventricular dysrhythmias lead to sudden death •Left heart failure is cause of death in 75% of individuals with dilated cardiomyopathies •Ejection fraction is <40% •Majority of death occur in 5 years of diagnosis (only ~ 25% survive beyond 5 years)

-Functions of a nephron (3)

-filtration: Which is the movement of plasma across a filtration membrane (Bowman's capsule) due to a pressure gradient.-reabsorption: Movement of substances from the filtrate (urine) back into the blood • This is the way the body recovers the salt, water, and other nutrients it needs -secretion: active transport of substances into the nephrons for excretion. This helps refine the ion concentrations in the body to maintain blood homeostasis

Myocarditis

-inflammation of heart muscle & conduction system without evidence of coronary artery disease or MI. Most often it is a result of viral infections of the myocardium (but bacterial and fungal infections can also be culprits). -the viruses the ones that are the most important cause of myocarditis in north America and Europe are the coxsackie viruses and other enterovirus - these usually manisfest as flu-like symptoms hint, hint***

Cardiogenic shock

-occurs when the heart fails to pump blood effectively through the body's organs and tissues -Decreased CO, Hypotension, hypoperfusion, indications of tissue hypoxia -may occur suddenly from causes like MI (damage to LV), myocardial contusion, sustained arrhythmia's, and cardiac surgery. -may ensue as an end-stage condition of CAD or cardiomyopathy -Treatment aims to strike balance between improving CO and reducing workload and oxygen needs of myocardium and increasing coronary perfusion.

Frank-Starling law

-there is a direct relationship between the volume of blood in the heart and the stretch or length of cardiac fibers at the end of diastole and the force of contraction during the next systole in a normal functioning heart. The failing or dilated heart may not be able to respond to increased filling because its fibers are already lengthened maximally. -Frank-Starling law of the heart describes how the heart adjusts its pumping strength (contractile force) in response to changes in the amount of blood returning to it.

Atherosclerosis (2)

-therosclerosis is a slowly progressive disease and is a form of arteriosclerosis, in that it is a narrowing and thickening of the blood vessel wall...but...it is caused by the accumulation of lipid-laden macrophages within the arterial wall. This then leads to the formation of a lesion known as a plaque -Atherosclerosis is not a single disease but rather a pathologic process that can affect vascular beds throughout the body ischemic syndromes leading contributor to coronary artery disease (CAD) and cerebrovascular disease (see path map on next slide. -Inflammation of endothelium -cellular proliferation -Macrophage migration -LDL oxidation -fatty streaks form -Fibrous plaque develops -***inflammation with oxidative stress & activation of macrophages are the primary mechanism in atherosclerosis development***

Right heart failure

-• Failure of right heart to pump blood forward into the pulmonary circulation • Leading to accumulation or damming back of blood in the systemic venous side • Increase in right atrial, RV end-diastolic and systemic venous pressure -Causes: Persistent left-sided failure a failing left ventricle would cause blood to back up in the left atrium •And, then to the pulmonary circuit, right ventricle and right atrium • *** the main cause of right heart failure is left heart failure**** -Backward effects of right heart failure: •Increased venous pooling of blood •Edema of hands and feet •Ascites •Jugular vein distension •Hepatomegaly and splenomegaly - Forward effects of right heart failure: •Decreased pulmonary blood flow •Decreased blood oxygenation •Fatigue •Decreased systemic blood pressure (d/t decreased left heart filling d/t the decreased pulmonary blood flow)

4 MAIN causes of edema

1. Increased capillary hydrostatic pressure:increased pressure forces excessive amounts of fluid out of the capillaries into the tissues. Just remember it's the force that "pushes" fluid out 2. Decreased capillary oncotic pressure: loss of proteins in urine, nephrotic syndrome. Burns, wounds, failure to produce proteins (liver disease, malnutrition) 3. Increased capillary permeability: causes a localized edema and may result from an inflammatory response or infection. Usually the release of histamine and other chemical mediators released from injured cells cause increased cell wall permeability allowing proteins and fluid movement out of the vascular bed into the interstitium 4. Lymph obstruction: CA, Infection, surgery, congenital absence of lymph

Stable angina

Occurs when atherosclerotic coronary arteries cannot dilate to increase blood flow when oxygen demand is increased • Chronic coronary obstruction results in predictable chest pain is precipitated by physical activity, mental stress, and/or anger • Discomfort transient (3-5 minutes) and if blood flow restored no permanent damage • Pain is due to the build up of lactic acid or abnormal stretching of the ischemic myocardium that irritates the myocardial nerve fibers • Usually relieved by rest and nitro • *****Lack of relief may indicate developing infarction*****

Myocarditis

Of the viruses the ones that are the most important cause of myocarditis in north America and Europe are the coxsackie viruses and other enterovirus - these usually manisfest as flu-like symptoms

Abdominal aortic aneurysm

P-Lifting heavy weights straining Q-tearing knife like R- pain on Abdomen but boring through the back S very severe, and hits maximum at onset T Sudden onset -abnormal dilation or ballooning of the abdominal aorta, the largest artery in the abdominal cavity. AAAs can be serious and life-threatening if they rupture, but they often develop slowly and may not cause symptoms until they become large or rupture

HTN

Primary Hypertension specific cause not yet identified though thought to be combination of genetics and environment. Also, known as essential or idiopathic hypertension affects 90-95% of individuals with hypertension. The above is a path map showing the contribution of increased PVR and increased blood volume leading to sustained hypertension. -Genetic, environemntal, lifestyle -Endotherlial dysfunction, renin imbalance,

Lab considerations for extreme proteinuria

Protein: Remember we shouldn't see protein in urine as the molecules are to big to pass through the filtration membrane. So, if we see protein that's an indication that the glomerulus - -Protein-to-Creatinine Ratio (PCR): Normal Range: Less than 0.15 grams of protein per gram of creatinine Microalbuminuria: 0.15 to 2.99 grams of protein per gram of creatinine Macroalbuminuria: 3 grams of protein per gram of creatinine or higherHemoglobinuria seen during states of hemolysis blood transfusions, incompatibilities, elevated hgb •Myoglobinuria seen with ischemia, crush injury protein that makes up muscle...urine will look tea color, brownish, can precipitate in tubules breakdown products are toxic -**just know that FeNa is a test used to help indicate what type of failure the patient may have.

Pulmonary congestion

accumulation of fluid in the lung tissues and airspaces. This condition can make it challenging for the lungs to function effectively in oxygenating the blood and can lead to significant breathing difficulties. Pulmonary congestion can be a symptom of various underlying medical conditions, and it is essential to identify and treat the root cause to alleviate the congestion. Here are some key points about pulmonary congestion:

Renin

an enzyme produced by the juxtaglomerular cells of the nephrons. Which are cells are located in the walls of the afferent arteriole. They act as baroreceptors (responding to renal blood flow)

ADH

antidiuretic hormone (vasopressin) It has an effect on blood vessels causing vasoconstriction increasing BP 5. It has an effect on the kidney by increasing the permeability of the distal tubule and collecting duct membrane to water, so.... It increases reabsorption of water increasing blood volume •Because of increased water reabsorption from the filtrate the urine becomes more concentrated •And there's a decrease in the amount of urine produced *Diabetes insipidus (insufficient ADH) *SIADH (Too much ADH)

Prinzmetal (variant) angina

occurs due to abnormal vasospasm of coronary vessels resulting in unpredictable chest pain • occurs almost exclusively at rest, at night during REM sleep • this abnormal vasospasm of one or more major coronary arteries can be with or without atherosclerosis • may be d/t hyperactivity of sympathetic nervous system, or increased calcium influx into arterial smooth muscle • ****if spasm persists infarction results**** •Treated with nitroglycerin and Calcium antagonists

Post-renal failure

occurs secondary to obstruction of urine. Urine is being produced but there's problems with elimination of the urine. Obstruction can occur at level of ureter, bladder, urethra Most common reasons include:•Renal stones •Prostate hypertrophy •Ureter/urethral strictures •Ureter/urethral spasms •Neurogenic bladder •Horseshoe kidney

major site of reabsorption

proximal convoluted tubule

Renin-Angiotensin-Aldosterone System (RAAS)

regulates the ECF volume by regulating sodium content. Stimulation of this system leads to: 1. Systemic vasoconstriction 2. Sodium retention in kidneys (along with Na+ goes H2O) 3. Expansion of ECF volume

Right ventricular afterload

the resistance against which the right ventricle of the heart must pump blood to send it into the pulmonary circulation (lungs). The right ventricle is responsible for pumping deoxygenated blood from the body into the lungs, where it receives oxygen. The afterload in the right ventricle is primarily determined by the pressure in the pulmonary circulation, particularly in the pulmonary arteries

Preipartum cardiomyopathy

typically develops during the last month of pregnancy up to 5 months post partum. It is seen in ~ 1 per 3-4 thousand live births. 75% of the cases of peripartum cardiomyopathy is diagnosed within the first month post-partum (and 45% in the first week post-partum). Mortality is very high in this population with ranges of 18 - 50%. This cardiomyopathy resembles dilated cardiomyopathy. Risk factors are multifactorial advanced maternal age (over age of 30), preeclampsia, gestational hypertension.