Excretory System Flashcards
- Define obstructive uropathy.
Anatomic changes in the urinary system caused by obstruction
- Name 3 causes for obstructive uropathy.
Can be caused by kidney stones, compression from a tumor or inflammation, etc.
- Describe the time-related progress of disease with upper urinary tract obstruction.
Caused by kidney stones, tumours, inflammation
May occur in the ureter or within the kidney (pelvis) or nephron
Effect is time related: dilation and fibrosis occur first at the distal nephron (7 d), then the proximal nephron (14 d), and by 28 d, the glomeruli have been damaged and the cortex and medulla are reduced in size.
Irreversible damage can occur if the obstruction remains for 4 weeks, however, partially recovery can occur if the blockage is removed within 56 to 69 d.
- Describe the effect on the function of the kidney, and the effects on the body of upper urinary tract obstruction.
The kidney becomes unable to conserve sodium, bicarbonate and water, and excrete hydrogen and potassium ions, leading to dehydration and metabolic acidosis.
- Describe compensatory hypertrophy and hyperfunction.
If one kidney is obstructed, the body can compensate: in the unobstructed kidney the size of individual glomeruli and tubules is increased, but not the total number of functioning nephrons.
In this way, the unobstructed kidney can make up for the reduction in function of the obstructed kidney.
This ability decreases with age, and the process is reversible if obstructed kidney recovers.
- Define “calculi”.
Kidney stones
- What are the most common kidney stones composed of and where can they be located?
- What is the immediate cause of calcium oxalate or phosphate kidney stones and what are 2 causes of this immediate cause?
Can be formed of crystals, proteins or other substances and located in the kidneys, ureters and urinary bladder.
Influenced by factors including: age, fluid intake and diet
Most common stones are composed of calcium oxalate or phosphate (70%-80%), due to factors including high urine calcium, caused by hyperabsorption of calcium from the intestines or hyperparathyroidism
Stones smaller than 5 mm have about a 50% chance of spontaneous passage, whereas stones that are 1 cm have almost no chance of spontaneous passage.
- What is renal colic?
- What is useful about the location of renal colic
- How are urinary calculi treated?
Renal colic is described as moderate to severe pain (can be incapacitating, with nausea), the location of which can indicate where the obstruction is in the ureter (e.g., originating in the flank pain and radiating to the groin (obstruction of renal pelvis or proximal ureter) vs radiating to the lower abdomen (midureter))
Treatment includes removing stones, managing pain, reduction of further formation through increasing fluid flow and altering diet.
- What is lower urinary tract obstruction primarily related to?
Primarily related to storage of urine in the bladder or emptying of urine through the bladder outlet.
- Describe neurogenic bladder – what does the type of dysfunction depend upon?
- Name two physical obstructions of the lower urinary tract.
Neurogenic bladder (743)– bladder dysfunction caused by neurologic disorders. The type of dysfunction (whether incontinence or functional obstruction) depends upon where damage has occurred in the nervous system (CNS vs peripheral nerves). Physical obstruction (745) - Scarring of the urethra (infection, surgery), enlarged prostate
- Define glomerulonephritis.
- Identify the two common immune mechanisms that can lead to glomerulonephritis.
- Describe the series of steps in the development of glomerulonephritis as caused by these immune mechanisms.
Glomerulonephritis – inflammation of glomerulus caused by immunologic responses, infection, diabetes mellitus, etc.
Immune mechanisms are most common cause, either Type III (deposition of circulating Ab/Ag complexes into the glomerulus) or Type II (Ab reacting against Ag within the glomerulus). Ab activate complement proteins, which summon macrophages and neutrophils, which secrete compounds that damage the glomerular cells. This increases membrane permeability, which allow proteins and RBC to escape into filtrate. Proteinuria and/or hematuria develop.
- Define nephrotic syndrome.
2. Define nephritic syndrome.
Nephrotic syndrome (nephrosis) – excretion of 3.5 g or more of protein/day in urine, characteristic of glomerular injury (due to certain forms of glomerulonephritis, vascular disorders, diabetes mellitus, etc).
Nephritic syndrome – excretion of blood cells in addition to protein (not as much protein as in nephrosis). Is also due to alterations in glomerulus, due to inflammation.
- Define BUN – what two facts does it reveal about the state of the kidney?
BUN – blood urea nitrogen – concentration of urea in the blood. This reflects glomerular filtration (because urea is filtered at the glomerulus, as filtration drops, BUN rises) and urine-concentrating capacity (because urea is reabsorbed from the nephron, if flow through nephron decreases (due to dehydration or renal failure, BUN rises)).
- What does the level of creatinine in the plasma reveal about the state of the kidney?
Plasma creatinine concentration – creatinine is produced by the muscles, is filtered at the glomerulus, and never reabsorbed. Because of this, it indicates the amount of filtration that is occurring at the glomerulus. If the glomerular filtration rate decreases, the plasma creatinine concentration increases and vice versa.
- Define AKI (include BUN and plasma creatinine).
Sudden decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood (increased BUN and plasma creatinine).
- What does “RIFLE” represent in terms of acute kidney injury?
Spectrum is described by “RIFLE” criteria (based on glomerular filtration rate and urine output): Risk – Injury – Failure – Loss – End stage disease
- What is prerenal AKI caused by and give an example of one condition that would lead to this.
- What does intrarenal AKI result from and give an example of an event/condition that would lead to this.
- What does postrenal AKI result from and give an example of one condition that would lead to this.
Most common reason for AKI
the decrease in GFR is caused by renal hypoperfusion.
Lowered hypoperfusion may be due to renal vasoconstriction, hypotension, hypovolemia, hemorrhage or inadequate cardiac output.
If pressure continues to be low, lack of oxygen delivery can cause cell injury and necrosis.
Intrarenal acute kidney injury (755)
Usually results from tubular necrosis as a result of occurrences including: prerenal injury, ischemia after surgery), exposure to toxins (e.g., carbon tetrachloride), glomerulonephritis, vascular disease (DIC), allograft rejection, tumor growth.
- Postrenal acute kidney injury (755)
Urinary tract obstructive disorders
Rare, usually occurs with urinary tract obstruction that affects both kidneys (e.g., neurogenic bladder)
Causes an increase in pressure upstream, resulting in decreased GFR
- Describe the 3 stages of AKI.
- Define oliguria and when it may occur with AKI.
- What 3 measures are taken to treat AKI?
Initiation: reduced perfusion or toxicity in which the kidney injury is evolving. Possible to reverse.
Maintenance: kidney injury has been established – dysfunction may last from weeks to months. Urine output is the lowest and serum creatinine and blood urea nitrogen (BUN) levels both increase
Recovery: interval when kidney injury is repaired – normal renal function occurs.
Oliguria (low output of urine) begins within 1 day after a hypotensive event and lasts 1-3 weeks, depending upon the duration of ischemia/severity of injury
Oliguria may not occur with some AKI (those associated with nephrotoxins), but plasma creatinine and blood urea nitrogen (BUN) levels will increase.
Primary goal of therapy is to maintain life until renal function has been recovered:
Correct fluid and electrolyte imbalances
Treat infections
Maintain nutrition
Remember that drugs and metabolites are not excreted
Continuous renal replacement therapy (e.g., dialysis, kidney transplant) may be required
- Define chronic kidney disease, and name one disease with which it is associated.
Refers to a declining glomerular filtration rate; a progressive loss of renal function
= “chronic renal failure”, “renal insufficiency”
Associated with systemic disease, such as hypertension, diabetes mellitus, chronic glomerulonephritis, obstructive uropathies, etc.
- What does the intact nephron hypothesis propose?
Symptoms of CKD do not actually become apparent until renal function declines to less than 25% of normal.
Up to this point, adaptations have occurred to the loss of nephron mass
The intact nephron hypothesis proposes that the unaffected nephrons are capable of hypertrophy and hyperfunction in their rates of filtration, reabsorption and secretion, in order to make up for the declining GFR
- How does the urine of a person with CKD compare to that of a person with normally functioning kidney?
Due to this compensation, although the urine of a person with CKD may contain abnormal amounts of protein and blood cells, the major end products of excretion are similar to those of normally functioning kidneys until the advanced stages of renal failure, when there has been a large loss of functioning nephrons.
- Define azotemia.
2. Define uremic syndrome (uremia).
Azotemia = increased levels of serum urea and other nitrogenous compounds related to decreasing kidney function. Uremic syndrome (uremia) = the systemic symptoms associated with the accumulation of nitrogenous wastes and toxins in the plasma.
- Fluid, electrolyte and acid/base balance are disturbed by CKD. Describe how each of the following is affected: sodium, potassium, creatinine and urea, pH, calcium, proteins and fat.
Sodium – Ultimately, the kidney loses its ability to regulate sodium and water, and both are retained, contributing to edema (“anasarca” = a general accumulation of fluid in body cavities and tissues) and hypertension.
Potassium – In later stages, potassium is not secreted sufficiently and can increase to life-threatening levels.
Creatinine and urea levels in the plasma increase as GFR decreases
Metabolic acidosis: The kidney’s ability to secrete hydrogen ions and reabsorb bicarbonate ions is decreased.
Calcium: less calcium is absorbed from the GIT. WHY??. This is detected by the parathyroid gland, which then increases levels of PTH, which results in loss of calcium from the bone, increasing the risk of bone fracture.
Proteins and fat: advanced CKD causes decreases in amount of proteins (loss of muscle mass and serum proteins). There is also a shift in the ratio of LDL/HDL, with more LDL, causing increased atherosclerosis
- Describe the effects on each of the following body systems: cardiovascular, pulmonary, hematologic, immune, neurologic, gastrointestinal, endocrine and reproductive.
Cardiovascular system
Major cause of death in CKD
Excess sodium and water lead to hypertension
Excess LDL leads to increased atherosclerosis
Kidney produces less erythropoetin, so anemia may result, increasing cardiac workload
Pulmonary system
Complications associated with fluid overload
Acidosis results in Kussmaul respirations
Hematologic system
Anemia, impaired platelet function
Neurologic system
Headache, pain, drowsiness, impaired concentration and memory loss – with later stages, seizures and coma
Gastrointestinal system
Anorexia, vomiting, constipation or diarrhea
Endocrine and reproductive systems
Decrease in levels of sex steroids bring symptoms such as impotence, amenorrhea
Insulin resistance can occur, as well as alterations in thyroid hormone metabolism
