Module 8 - The Renal System Flashcards

1
Q

Describe the different parts and functions of the nephron

A

The nephron is the basic structural and functional unit of the kidney. The function is to control the concentration of water and soluble materials by filtering the blood, reabsorbing needed materials, and excreting waste products as urine. The nephron eliminates wastes from the body, regulates blood volume, pH and pressure, and controls the levels of electrolytes.

It is made of the renal corpuscle and tubules. The renal corpuscle is made of the glomerulus and the glomerular capsule/Bowman’s capsule. The glomerulus is a capillary bed that allows the fluid of the blood solutes and small molecules to flow out of the blood vessels or the capillary. Once it is out of the capillary and into the surrounding corpuscle, it’s called filtrate.
The glomerular/Bowman’s capsule is a cup shaped chamber to hold filtrate; as it is collected, it will then be able to flow through the rest of the tubular nephron.

The renal tubules modify filtrate to create urine. Filtrate first moves through the proximal convoluted tubule (PCT) which has the largest role in reabsorbing nutrients. Then through the loop of Henle , which establishes an osmotic gradient that will allow for water reabsorption and concentration of the urine. Then to the Distal convoluted tubule (DCT) which functions to futher modify the tubule fluid through excretion or reabsorption. The cells of the DCT contain aldosterone receptors to help with regulating blood pressure by creating osmotic gradients.

Each DCT links to the collecting ducts that capture the tubular filtrate from the nephrons, then passes the fluid to the medulla (middle of kidney), and then eventually concentrates the urine and it flows out of the kidney into the ureter.

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2
Q

Explain glomerular filtration, tubular reabsorption, and tubular secretion.

A

In glomerular filtration, the glomerulus (capillary bed) has fenestrated capillaries with filtering holes that allow plasma to be pushed out via hydrostatic pressure and that plasma contains water and solutes. The fenestrations are small enough that no blood cells or proteins should leave. The normal glomerular filtration rate (GFR) is 120 mL/min.

Tubular reabsorption is the movement of substances that have just been secreted from the blood into the filtrate, it is taken back into the bloodstream - generally electrolytes, glucose, bicarbonate, and amino acids.

Tubular secretion is the movement of substances from the bloodstream in the vasculature that runs around the nephron to the filtrate in the tubules. This is often water, H+ to control pH.

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3
Q

Chemically, how does reabsorption occur?

A

There are transporters on the lumen side of the proximal tubular cell. As fluid moves by, they can take back particles that are in it. A transporter brings sodium in from the tubular lumen, into the cell, and into the capillary blood. As the transporter brings the sodium, it will also be bringing back glucose and amino acids. On the opposite (vasolateral) side of the bloodstream, we have other transporters, as well. We have a sodium potassium ATPase pump. As sodium comes ito the cell, it is quickly shuttled out into the blood, and so we are setting up a concentration gradient here. As we constantly shuttle sodium out, then the lumenal side transporter is going to be pulling sodium into the concentration gradient, and it will pick up glucose and amino acids as well, bringing them back into the bloodstream

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4
Q

List the three ways the kidney acts as an endocrine organ

A

Through the renin-angiotensin-aldosterone system
Through the regulation of red blood cell production through the formation of erythropoietin (EPO)
Through calcium metabolism by the activation of vitamin D

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5
Q

Describe the action of ADH

A

ADH acts on the collecting tubules to increase water absorption. ADH inhibits urine output by increase the number of water channels in the cell membrane of the collecting ducts.

Antidiuretic hormone (ADH)- made by the hypothalamus and it is released by the posterior pituitary gland. It’s triggered by an increase in the blood’s osmolality. It’s also triggered by the RAAS system (renin-angiotensin II - aldosterone - system) which is activated by hypotension. The angiotensin II that is produced, can cause a release of ADH. And so after ADH is released, it travels to the collecting ducts and it places pores in the cells surface, and that allows water to move from the collecting duct back into the bloodstream. As it does so it would be increasing the blood’s volume again to help raise our bloodpressure. At the same time it decreases the volume of the filtrate in urine, and by doing so it would be concentrating the urine and making it a smaller volume

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6
Q

Describe the action of aldosterone

A

Aldosterone acts to place several types of ion channels inside the cells of the collecting ducts. One type of ion channel is a sodium-hydrogen ion channel. Aldosterone increases Na+ reabsorption through the excretion of H+ ions. Na+ ions are pumped out of the filtrate while hydrogen ions are pumped inside and then excreted. Because water follows salt, Na+ reabsorption will cause water reabsorption. Aldosterone will also increase K+ secretion through Na+/K+ pumps. Na+ is pumped out of the filtrate to be returned to the blood while potassium (K+) is excreted in urine. The main action of aldosterone is to increase the blood volume and, therefore, blood pressure when needed.

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7
Q

Describe how RAAS helps to maintain the GFR

A

Hypotension or hypovolemia (decrease in blood volume) is going to decrease the renal profusion of blood and so when we have the decrease of blood pressure, we have different receptors by the kidney that can detect it. So first, we have the blood vessels that lead into the glomerulus - afferent blood vessels. They have stretch receptors, and they can pick up on that decrease in stretch and that signals to them there is a decrease in blood pressure.
We also have chemoreceptors in the cells close to the glomerulus. These are going to be the macula densa cells. They can pick up on when there is a decrease in NaCl delivery. They are screening for the presence of those ions. And so if there’s less coming through, they detect there’s less blood/blood pressure, these signals signal to the kidney to release RENIN - the hormone that the kidney can control and release.
Renin is a prohormone, it has to be processed. The process happens in different places, so the renin substrate is going to be cleaved into angiotensin I in the bloodstream. It travels and comes to the lungs where we have ACE (angiotensin converting enzymes) that will cleave it into its final active form, angiotensin II
Angiotensin II is going to act in a few different ways:
It can trigger thirst, vasoconstriction
Releases other hormones
Angiotensin II is going to trigger aldosterone secretion which is a hormone that is going to work in the distal convoluted tubule (DCT) and take back sodium. As we take back sodiu, water is going to follow it by those osmotic principles, so we will reabsorb more water. As we do so, we’ll have an increase in our blood volume and hopefully raise the blood pressure.
Agiontensin II also causes our antidiuretic hormone to be released which will cause water to be reabsorbed as well. And Angiotensin II via vasoconstriction is also going to work to raise the blood pressure.
As these mechanisms take place, there will be a decrease of renin released because we’ll be coming back into our homeostatic balance, but as the blood volume and pressure increase, we will be able to maintain that GFR, which is so important for the kidneys and their function.

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8
Q

Compare and contrast the renal cortex and renal medulla. Discuss the structures found in each.

A

The outer cortex houses the glomeruli and convoluted tubules (proximal and distal) of the nephron as well as blood vessels. The inner medulla is comprised of the Loop of Henle of the nephron and cone-shaped masses also known as the renal pyramids.

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9
Q

Explain the difference between cortical nephrons and juxtamedullary nephrons.

A

Cortical nephrons make up 85% of all nephrons. They originate superficially in the cortex and have shorter loops of Henle that extend only a short distance into the medulla. Juxtamedullary nephrons make up the remaining 15% of all nephrons. They originate deeper in the cortex, and their loops of Henle are thinner and extend into the medulla entirely.

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10
Q

Explain the differences in the two systems providing the blood supply to the nephron. How does their structure determine their role?

A

The glomerulus is located between afferent and efferent arterioles, which are high resistance vessels resulting in an extremely high pressure system which can easily force fluid and solutes out of the blood into the glomerular capillary along its entire length. This allows blood to flow into the glomerulus to be filtered.

The peritubular capillaries are low pressure vessels better suited for reabsorption as opposed to filtration. These capillaries are surrounded by tubules in their entirety allowing rapid movement of solutes and water. Efferent arterioles located deep in the renal cortex turn into long, thin-walled vessels known as the vasa recta, and they run parallel to the loops of Henle in the medullary region and assist in the exchange of solutes and water flowing in and out of the kidney.

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11
Q

Name two specialized structures of the glomerular capillaries that contribute to the filtration of blood.

A

Fenestrations and podocytes

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12
Q

What is the norm value for the GFR? Discuss why maintenance of this value is important.

A

A normal glomerular filtration rate (GFR) is 120-125 ml/min or 180 L/day. Maintenance of a relatively constant GFR is important for adequate reabsorption of water and other needed nutrients from the filtrate.

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13
Q

List the 3 regulatory mechanisms of the GFR.

A

(1) renal autoregulation, (2) nervous system control, and (3) hormonal control.

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14
Q

What are common tests for kidney function?

A

Urinalysis - test strip can determine pH, presence of protein or glucose (damage to the kidneys or hyperglycemia), white blood cells or nitrites (infection in urinary tract), bilirubin (liver problem), and blood (infection or kidney damage).

Estimated glomerular filtration rate (eGFR) - estimated by timed samples of blood and urine screened for the waste product creatinine, which is a waste product from muscle metabolism and it gets filtered out of the blood and is not reabsorbed into the body, so it should be secreted at a steady rate.

Blood Urea Nitrogen (BUN) - indicates health of kidneys and liver. When proteins are broken down into amino acids, ammonia is produced and then converted into less toxic urea by the liver. If there’s an increased amount of urea - the liver is producing more or the kidneys are not filtering it out as they should. If there’s a decrease, the liver is not functioning properly and producing the urea.

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15
Q

Describe the three layers of the glomerular capillary membrane

A

The glomerular capillary membrane contains 3 layers: (1) the capillary endothelial layer, (2) the basement membrane, and (3) the single-celled capsular epithelial layer. The endothelial cells contain small pores called fenestrations which allow for the filtration of blood. The epithelial layer surrounding the glomerulus is continuous with the epithelium that lines Bowman capsule. Podocytes (foot processes) are long extensions of the epithelium that embed themselves into the basement membrane. The podocytes form small pores referred to as slit pores which allow the glomerular filtrate to pass. See Figure 8.3B. The basement membrane is situated between the epithelial and endothelial cell layers as seen in Figure 8.3C. Spaces within the structural framework of the basement membrane determine the size-dependent permeability of the glomerulus. The size of these spaces, under normal circumstances, prevent red blood cells and plasma proteins from passing through the glomerular membrane into the filtrate. A compromise to the basement membrane would lead to the leakage of red blood cells and proteins into the filtrate which occurs with glomerular disease.

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16
Q

Define hyponatremia using blood values.

A

Hyponatremia occurs when plasma concentration falls below 135 mEq/L.

17
Q

Define hypernatremia using blood values.

A

Hypernatremia occurs when plasma Na+ levels rise above 145 mEq/L with a serum osmolality greater than 295 mOsm/kg.

18
Q

Define hypokalemia using blood values.

A

Hypokalemia occurs when plasma K+ levels fall below 3.5 mEq/L.

19
Q

Define hyperkalemia using blood values.

A

Hyperkalemia occurs when plasma K+ levels rise above 5 mEq/L.

20
Q

Define hypocalcemia using blood values.

A

Hypocalcemia is the result of Ca2+ levels falling below 8.5 mg/dL.

21
Q

Define hypercalcemia using blood values.

A

Hypercalcemia occurs when plasma Ca2+ levels are greater than 10.5 mg/dL.

22
Q

Define hypomagnesemia using blood values.

A

Hypomagnesemia occurs when plasma Mg2+ concentration is less than 1.8 mg/dL.

23
Q

Define hypermagnesemia using blood values.

A

Hypermagnesemia is the result of blood Mg2+ levels rising above 3.0 mg/dL.

24
Q

What are the 3 mechanisms of control for blood pH.

A

Blood pH is controlled by three main methods in the body: (1) the chemical buffer systems, (2) the brainstem respiratory center, and (3) the renal system.

25
Q

Be able to list and describe the 4 types of kidney stones.

A

Calcium stones are a result of increased concentrations of calcium in the blood and urine. This can occur secondary to increased bone resorption, typically associated with immobility, bone disease, or hyperparathyroidism.

Magnesium ammonium phosphate stones form in urine that is alkaline (pH>7.) This increase in pH is the result of a UTI caused by bacteria possessing an enzyme called urease. Urease will break urea into ammonia and carbon dioxide. The ammonia will form an ammonium ion which increases the pH of the urine. The resulting stones increase in size as the levels of bacteria rise. These types of stones account for approximately 15% of all kidney stones.

Uric acid stones typically coincide with gout. These stones form when the pH of urine is more acidic. Unlike calcium stones, uric acid stones are not visible on x-ray films. They account for approximately 7% of kidney stones.

Cystine stones are rare, making up approximately 1-3% of all kidney stones. However, they are the most common cause of stones among children. They are a result of cystinuria. Cystinuria occurs when there is a decrease in tubular absorption of cystine, a result of a genetic defect in renal transport.``

26
Q

What are the common causes of acute postinfectious glomerulonephritis?

A

Acute Postinfectious Glomerulonephritis occurs as the result of another infection including streptococcus and staphylococcus bacterial infections, viral infections such as hepatitis, and even parasitic infections.

27
Q

Be familiar with various diagnostic tests and treatments for renal Calculi.

A

Urinalysis, x-rays, CT scan, intravenous pyelogrpahy, and abdominal ultrasound.

Urinalysis looks at urine pH, stone forming crystals, infection, or hematuria.

28
Q

What are the 3 categories of acute renal failure?

A

Prerenal - most common; decreased renal blood flow.

Postrenal failure is when the outflow of urine from the kidney is impeded.

Intrarenal failure/acute kidney injury - caused by conditions that damage structures within the kidney, namely glomeruli, vessels, tubules, or the interstitium.

29
Q

What are the 2 types of ATN?

A

Ischemic acute tubular necrosis occurs most frequently among patients who have had major surgery or suffered trauma or burns. Damage to the tissue releases toxins that make the tubular cells more susceptible to ischemic effects.

Nephrotoxic ATN is brought on by exposure to drugs and other nephrotoxic agents. This exposure injures the tubules direction, through renal vasoconstriction, or by producing a tubular obstruction.

30
Q

What are the 3 phases of ATN?

A

The onset or initiating phase of ATN (hours/days) is the time between the precipitating event/exposure (i.e. ischemic event or toxin exposure) and tubular injury.

The maintenance phase is marked by a drastic decline in the GFR. This causes the retention of metabolites that are cleared by the kidney under normal conditions. Urine output is at its lowest at this point. Fluid retention will lead to edema, water intoxication, and pulmonary congestion. If this phase is prolonged, hypertension will develop as well asl uremia. If this goes untreated, seizures, coma, and even death can result.

The recovery phase of ATN is the period in which tubular repair takes place. Urine output will increase and there will be a fall in blood creatine levels. Diuresis (increased or excessive urine production) may occur during this phase and can cause excessive water and electrolyte loss. Eventually tubular function is restored as well as BUN and creatine levels.

31
Q

What blood values are closely monitored in renal failure?

A

BUN and creatinine levels.

32
Q

Describe the process of Hemodialysis.

A

Blood circulates through the hollow dialyzer composed of bundles of capillary tubes. Dialysate (dialysis fluid) moves on the outside of the tubes. The walls of these capillary tubes are composed of semipermeable material which allows all molecules (except blood cells and plasma proteins) to move in both directions (from the blood into the dialysate and from the dialysate into the blood). Waste products will diffuse into the dialysate. During dialysis treatments blood will flow from the patient’s artery through the blood chamber of the dialysis machine (where it is filtered) and back into the patient’s body through a vein. Vascular access is achieved through a shunt (implantation of tubing into an artery and vein) or more commonly through an arteriovenous fistula (anastomosis of an artery to a vein). Patients are put on blood thinners such as heparin to prevent blood clotting during treatment. Common symptoms that accompany dialysis treatment include nausea, vomiting, muscle cramps, headache, chest pain, and vertigo. Treatments are usually done 3 times each week and last 3-4 hours.

33
Q

Describe the process of peritoneal dialysis.

A

Peritoneal dialysis utilizes the same principles of hemodialysis; however, the serous membrane of the peritoneal cavity serves as the dialyzing membrane. A catheter is surgically placed in the peritoneal cavity and is tunneled through subcutaneous tissue to its exit on the side of the abdomen. A sterile dialyzing solution is run through the catheter over a period of 10 minutes. The fluid will remain in the peritoneal cavity for a prescribed amount of time allowing metabolic waste products to diffuse into the solution. At the end of this time, the fluid is drained from the peritoneal cavity into a sterile bag. This type of dialysis can be at home, but infection is a concern at the catheter exit site.

34
Q

What are the determinants of transplantation success?

A

The overall health of the recipient, the degree of compatibility between the donor and the recipient, and the management of recipient immunosuppression.

35
Q

What is the RAAS impact on blood volume

A

RAAS increases blood volume.

Angiotensin II: increases thirst, increases ADH and aldosterone
ADH : reabsorption of water
Aldosterone: reabsorption of sodium (water will follow) and excretion of potassium (concentrate urine)

36
Q

What is an acid/base/pH

What is acid-base balance

A

An acid is a hydrogen donating compound that dissolves in water to release hydrogen ions.

A base is a compound that can accept a hydrogen ion

pH is the measure of hydrogen ion concentration in a solution.

Acid-base balance means that the body generates H+ and eliminates or stores them in an equal amount to maintain its balance.

37
Q

What are the ways that H+ is regulated

A
  1. Chemical buffer systems - rapid; first line of defense. It consists of a weak base and its conjugate acid pair or a weak acid and its conjugate base pair. Buffer systems work by shifting a reversible chemical reaction by mixing the weak acid and base to inhibit fluctuations in pH. Compounds that can act to resist pH changes by binding to hydrogen with the pH drops and it can release the hydrogen so the pH rises. The bicarbonate buffering system - interstitial and plasma fluids; weak carbonic acid and weak bicarbonate ion. The phosphate system - urine and intracellular fluid; weak acid phosphate and monohydrogen phosphate ion. The protein system - intracellular fluid; proteins can function as an acid or base and contain many ion groups that can release or bind H+.
    These chemical buffer systems react to minimize changes in pH by binding free H+ or free OH-.
  2. Respiratory regulation of H+: within 1-3 minutes. In the lungs, carbonic acid can break down into water and CO2 and then the lungs can breathe out and get rid of the CO2. Alternatively, if the lungs retain the CO2 it will decrease our body’s pH. If the chemoreceptors detect an increase in pH (indicating blood alkalinity), the respiratory center is depressed, causing hypoventilation. During hypoventilation, the respiratory rate slows down allowing CO2 to accumulate. Following the above reaction, as more CO2 accumulates it combines with water to form H2CO3. As carbonic acid dissociates (reaction moving to the right) more H+ ions are formed which increases the acidity, and the normal blood pH is thus restored.
  3. Renal mechanisms: most potent, but hours to days. The kidneys can eliminate acids like phosphoric, uric, and lactic acids as well as hydrogen ions. The kidneys can also generate buffer like bicarbonate that combines with excess hydrogen and can help raise the pH. The kidneys play three roles in regulating acid-base balance. The first is through the excretion of H+ from acids that are byproducts of protein and lipid metabolism. The second is through the reabsorption of HCO3- that is filtered in the glomerulus to keep it from being excreted in the urine. The third is the synthesis of new HCO3- that is then released back into the blood.

CO2 can diffuse into the tubule cells and diffuse from the urine or blood or body. Once here, carbonic anhydrase can catalyze the reaction for carbon dioxide + water to make carbonic acid. The carbonic acid can then break down and as it does it makes a hydrogen ion and bicarbonate. Bicarbonate is going to be reabsorbed so it can go buffer hydrogen ions in the body and this excess hydrogen will be excreted into the urine. And we can get rid of it that way.

38
Q

How do we diagnose acid-base imbalances

A

Arterial blood gas - blood is drawn from an artery so we measure highest content of oxygen and from that we assess pH, oxygen, CO2, and bicarbonate levels of the blood.

Anion gap (blood and urine) - assessment of different electrolytes in the blood. Cations (sodium and potassium) minus anions (chloride and bicarbonate) = the difference equal unmeasured anions that are generally phosphates, sulfates, proteins, and organic acids. It’s used for measuring metabolic acidosis.

39
Q

How do you determine if someone is in acidosis or alkalosis

A

To determine if someone is in acidosis or alkalosis you must first look at their pH level. You would then determine whether the primary cause of their disorder is respiratory or metabolic in nature by evaluating CO2 and HCO3- values. Finally, if there are multiple abnormal values, it is necessary to determine if one of the abnormal values is due to compensatory mechanisms.
Acidosis characterized by pH < 7.35 with an abnormally high PCO2 (> 45 mm) is respiratory acidosis. If renal compensation is occurring, HCO3- concentration will be > 26 mEq/L as the renal system attempts to raise the pH by increasing HCO3- concentration.
Acidosis characterized by pH < 7.35 with an abnormally low HCO3- concentration (< 22 mEq/L) is metabolic acidosis. If respiratory compensation is occurring, the PCO2 will be < 35 mm as the respiratory system attempts to raise the pH by decreasing PCO2.
Alkalosis characterized by pH > 7.45 with an abnormally low PCO2 (< 35 mm) is respiratory alkalosis. If renal compensation is occurring, the HCO3- concentration will be < 22 mEq/L, as the renal system attempts to lower the pH by decreasing HCO3- concentration.
Alkalosis characterized by pH > 7.45 with an abnormally high HCO3- concentration (> 26 mEq/L) is metabolic alkalosis. If respiratory compensation is occurring, the PCO2 will be > 45 mm as the respiratory system attempts to lower the pH by increasing PCO2.