u7 Flashcards
BLOOD UREA NITROGEN
BUN
Blood urea nitrogen (BUN) – (Normal range = Less than 20) Urea is the by-product of protein metabolism in the liver. The ammonia formed in this process is synthesized to urea in the liver. Creation of BUN is the most important catabolic pathway for eliminating excess nitrogen in the human body. Measuring how much BUN is in the blood is an indicator of kidney damage. However, BUN is also affected by dehydration, so it only indicates kidney damage if Creatinine levels are also elevated.
CREATININE
Creatinine - a waste product from the normal breakdown of muscle tissue. As creatinine is produced, it is filtered through the kidneys and excreted in urine as a normal product of metabolism. If Creatinine is elevated in the blood that means it is not being excreted through the kidneys. An elevated creatinine along with an elevated BUN value, indicate kidney damage.
GLOMERULAR FILTRATION RATE GFR
Glomerular filtration rate (GFR). The GFR is 125 mL/min (normal range is 85-135 mL/min). It is a measure of how much blood (in mL) gets filtered by the glomeruli every minute. The GFR helps to detect kidney disease in its early stages more reliably than the creatinine test alone. GFR is affected by anything that would decrease the amount of blood flowing through the kidneys. This could include heart failure, atherosclerosis or hypotension, among other things.
UA
URINALYSIS
ABNORMAL SUBSTANCES
Urinalysis – A urine sample can provide a great deal of information about how the kidney is functioning. Urinalysis results include all of the following:
Specific Gravity (1.010 – 1.030) measures how dilute or concentrated the urine is. If the kidney is not functioning, the result will be a FIXED SPECIFIC GRAVITY, meaning the number stays the same through several tests. This indicates the kidney can no longer concentrate or dilute urine (kidney death).
Abnormal Substances: If ANY of these are found in the urine, it indicates a problem: RBCs (could be kidney stones, infection, bladder inflammation, kidney damage, etc.) WBCs (more than a few indicate the presence of infection) PROTEIN (kidney is damaged in some way and allowing large protein molecules to escape) GLUCOSE (if blood sugar is too high, glucose will “spill” into the urine) CASTS or crystals (pieces of mineral deposits that are breaking loose and being shed into the urine)
SPECIFIC GRAVITY
Specific Gravity (1.010 – 1.030) measures how dilute or concentrated the urine is. If the kidney is not functioning, the result will be a FIXED SPECIFIC GRAVITY, meaning the number stays the same through several tests. This indicates the kidney can no longer concentrate or dilute urine (kidney death).
URINE PROBLEMS
URIA’S
Azotemia - increased BUN and Creatinine (in the blood) WITHOUT systemic s/s
Uremia - increased BUN and Creatinine WITH multiple system organ failures
Polyuria – Increased urine output – could be due to a pathologic condition (such as diabetes)
or just increased fluid intake. In either case, the kidneys are not damaged!
Oliguria – decreased urine output (could be caused by dehydration or kidney failure)
Anuria – NO urine production (kidney failure)
PYELONEPHRITIS
PYELONEPHRITIS – See page 628 of Textbook
A potentially organ- and/or life-threatening infection that often leads to renal scarring. Bacteria usually reach the kidney by ascending from the lower urinary tract but may also reach the kidney via the bloodstream.
Causes – cystitis (UTI’s), urinary tract obstruction with reflux infection with E. coli, proteus, or pseudomonas
Epidemiology – FEMALES are 5 times more likely to develop acute pyelonephritis
PYLONEPHRITIS
READ
The most common cause of pyelonephritis is the backward flow (reflux) of infected urine from the bladder to the upper urinary tract. Bacterial infections also may be carried to one or both kidneys through the bloodstream or lymph glands from infection that began in the bladder. Kidney infection sometimes results from urine that becomes stagnant due to obstruction of free urinary flow.
A blockage or abnormality of the urinary system, such as those caused by stones, tumors, congenital deformities, or loss of bladder function from nerve disease, increases a person’s risk of pyelonephritis. Other risk factors include diabetes mellitus, pregnancy, chronic bladder infections, a history of analgesic abuse, paralysis from spinal cord injury, or tumors. Catheters, tubes, or surgical procedures may also trigger a kidney infection.
The bacteria most likely to cause pyelonephritis are those that normally occur in the feces. Escherichia coli causes about 85% of acute bladder and kidney infections in patients with no obstruction or history of surgical procedures. Klebsiella, Enterobacter, Proteus, or Pseudomonas are other common causes of infection. Once these organisms enter the urinary tract, they cling to the tissues that line the tract and multiply in them.
PYELONEPHRITIS - continued
Clinical Manifestations
Flank pain [Costovertebral (CVA) tenderness]
Fever/chills
Nausea/vomiting
Leukocytosis
Purulent urine (WBCs, bacteria and/or blood in urine)
2 MOST COMMON CAUSE OF LOC OF ELDERLY
UTI AND PNUEMONIA
ACUTE GLOMERULONEPHRITIS
ACUTE GLOMERULONEPHRITIS: Acute inflammation of the glomerular membrane. Primary cause - Untreated Group A streptococcal infection.
Clinical manifestations: (Evident in 10-15 days):
Acute hematuria
Proteinuria
Low serum albumin (see nephrotic syndrome)
Edema
Eventually oliguria
Other possible causes of glomerular injury
Drugs or toxins
Vascular disorders
Systemic diseases (diabetes mellitus, Lupus)
Viral infection
PATHOLOGY OF ACUTE GLOERULONEPHRITIS
Antibodies produced against strep organisms cross-react with glomerular endothelial cells
Immune complex (Ig G) formation of immune complexes (antigen/antibody complexes) in glomerulus (Type 3 Hypersensitivity).
Activation of complement (involved in the clotting cascade)
Recruitment of neutrophils and macrophages
Endothelial injury from free radicals and proteases
Inflammatory mediators cause increased glomerular membrane permeability
Loss of negative charge of basement membrane
Release of growth factors → diffuse endothelial and mesangial cell proliferation
Thickened glomerular membrane
Decreased GFR
Injury to the glomerulus, basement membrane, and glomerular capsule
NEPHROTIC SYNDROME
NEPHROTIC SYNDROME - See page 634 of Textbook.
Definition: Excretion of 3.5 gm or more of urinary protein per day
The kidney damaged by nephrotic syndrome has pores that allow molecules the size of a large protein to slip through – such as albumin – but will not allow anything larger (such as a red blood cell) to escape. Therefore, there is no hematuria present in this condition. The loss of protein in the urine cause low serum albumin levels.
Causes -
Glomerulonephritis
Genetic defects in the glomerular membrane
Systemic diseases (Diabetes, Lupus, etc.)
Drugs
Infections
READING ABOUT NEPHROTIC SYNDROME
PATHOPHYSIOLOGY & MANIFESTATIONS
Increased glomerular membrane permeability to protein → proteinuria
Loss of plasma proteins: Hypoalbuminemia → decreased oncotic pressure → full body EDEMA and fluid overload in the lungs/heart/brain.
Loss of immunoglobins → increased susceptibility to infection
Loss of specific transporter proteins (E.g. Decreased transport of vitamin D3 → decreased calcium absorption)
Hyperlipidemia: increased hepatic synthesis of lipids combined with decreased albumin levels
Increased LDL & VLDL → increased risk of atherosclerosis
Lipiduria (fats in the urine)
Study Question: What S/S would you expect to see if a person has lost protein through their urine as occurs in Nephrotic Syndrome? Answer: EDEMA. When kidneys are malfunctioning, the body retains water and causes full body edema (the Pillsbury Doughboy!). If really bad, even the area around the eyes fills with fluid and gets puffy (this is called PERIORBITAL EDEMA).
ACUTE TUBULAR NECROSIS
ACUTE TUBULAR NECROSIS (ATN) – See page 634 of Textbook.
Damage to the tubule cells of the kidneys, which can then lead to acute kidney failure. Acute tubular necrosis (ATN) is usually caused by a lack of oxygen to the kidney tissues (ischemia of the kidneys). It may also occur if the kidney cells are damaged by a poison or harmful substance.
ATN is one of the most common causes of ACUTE kidney failure in hospitalized patients*. In most people, ATN is reversible. The goal of treatment is to prevent life-threatening complications of acute kidney failure. Treatment focuses on preventing the excess buildup of fluids and wastes, while allowing the kidneys to heal. Patients should be watched closely for deterioration of kidney function.
RISKS FOR ACUTE TUBULAR NECROSIS
Risks for Acute Tubular Necrosis (ATN) include:
Low blood pressure (hypotension) lasting longer than 30 min.
Septic shock due to severe infection
Dye (contrast) used for x-ray studies
Medications that are toxic to the kidneys (such as aminoglycoside antibiotics or amphotericin)
Injury or trauma that damages the muscles (release of myoglobin from muscles → kidneys cannot filter this large molecule so it causes kidney damage)
Blood transfusion reaction
Recent major surgery
Signs and Symptoms of ATN
Central Nervous System: Change in LOC, confusion, delirium (due to Hypernatremia and cerebral edema)
Oliguria or anuria: due to severe kidney damage.
Full body EDEMA: due to fluid and sodium retention. Also due protein loss through tubules.
Cardiac Problems: due to potassium loss through the urine.
Fixed Specific gravity: LATE sign of END STAGE kidney failure.
