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132 Cards in this Set
- Front
- Back
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What is CVA?
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costovertebral angle - the point at which the bottom of the rib cage meets the spine and is commonly used as an external landmark for finding kidney position during physical examination
If there is pain, it recorded as CVA tenderness or flank pain. |
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How much liquid do the kidneys filter?
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The kidneys filter more than 7 L of fluid per hour, then reabsorb about 99%, producing a small amount of urine containing a high concentration of wastes.
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How much urine does the bladder collect?
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The urinary bladder collects 300-500 mL before stretch receptors signal a need for bladder emptying.
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What are the dimensions of the kidneys?
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The adult kidney weighs about 115-170 g; is 11 cm long, 6 cm wide, and 3 cm thick.
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What is the hilium?
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The concave portion of the kidneys which face the vertebral column
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What nervous system innervates the kidneys?
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The sympathetic division of the autonomic nervous system. It will constrict capillaries and react to blood pressure; SNS results in renal vasoconstriction and renin release. Pain receptors are present.
Absolutely no parasympathetic innervation. |
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How much cardiac output is directed to the kidneys?
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Approximately 25% of the cardiac output is delivered to the kidneys, the majority of which circulates through the cortex, while only 1-2% perfuses the medulla. Total renal blood to flow through the kidneys is about 1,200 mL/min.
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What are the three major functions of the kidneys/nephrons??
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1. filtration of water-soluble substances from the blood
2. reabsorption of filtered water, electrolytes, and nutrients (glucose, amino acids, proteins, and vitamins) 3. secretion of wastes or excess substances into the filtrate and formation of urine; secretion of hormones erythropoietin, renin, and vitamin D Also aids with acid-base balance. In addition to excreting excess hydrogen ions, the kidneys also regulate the concentration of bicarbonate (HCO3-) in the blood. The lungs and kidneys work together in maintain this balance. |
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Describe the composition of the nephron.
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Each nephron is composed of a glomerulus, which includes a capillary tuft and Bowman capsule, and a tubule, which includes the proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting tubule.
The nephron tubule is composed of a single layer of epithelial cells with an apical side facing the lumen and a basolateral side facing the interstitial space and capillaries. |
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What is GFR?
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Glomerular filtration rate is the rate of fluid filtration through the glomeruli into Bowman capsule per minute; normally 125 mL/min.
The main driving force for filtration is hydrostatic pressure in the glomerular capillaries. The most important physiologic regulator of GFR is blood volume. Increase fluid intake increases blood volume, increases BP slight, increases GFR. Glomerular capillaries are protected from fluctuations in BP by autoregulation (the arterial side of the body constricts or dilates depending on need). The GFR formula is determined by the filtration pressure in the glomeruli and by the permeable surface area of the glomerular membrane. (Don't need to know formula until post-licensure.) |
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What (the heck!) is hydrostatic pressure?
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Hydrostatic pressure is the pressure exerted by a fluid at equilibrium due to the force of gravity.
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So if the blood pressure drops, how does that affect hydrostatic pressure and GFR?
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A drop in BP that accompanies fluid loss results in drop in hydrostatic pressure and GFR. This triggers the hypothalamus to rapidly release ADH from the posterior pituitary.
ADH increases water reabsorption by the kidney by increasing water permeability of the distal tubules and collecting ducts. The BP drop also stimulates each juxtaglomerular apparatus to respond and secrete renin. This triggers formation of angiotensin II, which stimulates release of aldosterone from adrenal cortex, thus slowly boosting water reabsorption by kidneys by increasing reabsorption of sodium. |
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What is the function of the glomerulus?
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Filters fluid from the blood into Bowman capsule; prevents the passage of blood cells and proteins.
The glomerulus has the more permeable, thus most vulnerable to trauma, capillary in the entire body. |
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What is the function of the proximal convoluted tubule?
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Transports 2/3s of the filtered water and electrolytes and all of the filtered bicarbonates, glucose, amino acids, and vitamins from filtrate to interstitium.
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What is the function of the descending loop of Henle?
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Transports water, delivers a concentrated filtrate to the ascending loop of Henle.
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What is the function of the ascending loop of Henle?
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Actively transports sodium, potassium, and chloride to produce a hypo-osmotic filtrate and a high interstitial osmolality.
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What is the function of the distal convoluted tubule?
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Transports sodium, chloride, water, and urea; responsive to aldosterone; site of macula dense regulation of GFR; secretes hydrogen and potassium.
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What is the function of the collecting tubule?
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Passive transport of water under the influence of ADH; secretes hydrogen and potassium.
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What factors can affect GFR?
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When blood volume increases because of fluid intake, the blood pressure rises slightly and causes glomerular hydrostatic pressure to increase; GFR increases and the extra fluid is pushed into the filtrate to be excreted from the body. Also vice versa.
Obstruction in the tubules or collecting ducts can significantly elevate the pressure in Bowman capsule; GFR would fall because filtration pressure would be reduced. |
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Describe nephrogenic diabetes insipidus.
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When the collecting tubules are unresponsive to ADH, usually results from genetic defects in either the ADH receptor or the aquaporin 2 genes.
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What is renin?
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An enzyme stored and released by the juxtaglomerular cells; converts angiotensinogen to antiotensin I.
Renin is released in response to (1) decreased blood flow to the kidney, (2) reduced serum sodium levels, and (3) activation of sympathetic nerves to the juxtaglomerular cells. |
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What hormones is the kidney imperative for?
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Erythropoiein - a peptide growth factor that stimulates erythrocyte development in the bone marrow.
Vitamin D - synthesis of vitamin D is an interdependent function of the skin, liver, and kidney. It is a necessary cofactor for calcium absorption from the intestine and may also facilitate calcium reabsorption in the kidney tubules. In chronic renal failure, the production of active vitamin D is impaired, resulting in poor calcium absorption from the intestine and low serum calcium levels. |
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What lab tests are used to diagnose renal function?
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Urinalysis, serum creatinine, BUN, and GFR.
Kidney disease- CVA tenderness, UA, KUB, US, CT, MRI, biopsy. |
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Describe urinalysis.
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Urinalysis assesses urine color, clarity, odor, specific gravity, pH, glucose, ketones, protein, and sediment (including cells, crystals, casts, and bacteria or other organisms). The first urine void in the morning is the most concentrated, due to overnight fasting, and is the best specimen to use for a routine or baseline urinalysis, especially to assess pH, osmolality, and sediment.
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How much water is in urine?
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Urine is about 95% water and contains varying amounts of water-soluble waste products.
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Describe creatinine.
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Creatinine is an end product of muscle metabolism that is excreted exclusively by the kidney. Serum creatinine level averages about 0.7-1.5 mg/dL. It is slightly higher in men than women because of men's larger muscle mass.
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What is creatinine an indicator for?
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Serum creatinine is a fairly reliable indicator of renal failure because it is affected by only two factors: (1) the rate of creatinine produced from muscle, which is relatively constant in the absence of muscle breakdown, and (2) the rate of creatinine excreted by the kidney, which is determined by GFR.
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Describe urea.
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Urea is an end product of protein metabolism. It is excreted by the kidneys and measured in the blood as BUN.
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What is the normal range for BUN?
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10-20 mg/dL. It rises with a decrease in renal function, a decrease in fluid volume, and an increase in catabolism and dietary protein intake.
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What molecules should we NOT SEE in the urine normally?
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Shouldn't see protein, glucose, ketones, nitrites, casts, crystals. Also shouldn't see RBC or WBC, but if <5/HPF, it's ok.
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Which kidney is higher-positioned?
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The left kidney lies here at the 11th and 12th ribs. Because of the placement of the liver, the right kidney rests 1-2 cm lower than the left kidney and sometimes may be palpable.
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How do you assess for kidney inflammation?
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Make a fist, and hit the pt's back at CVA where kidneys are positioned. If pt cries, "Ouch," then the kidneys are inflamed.
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What major blood vessels are the kidneys attached to?
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Aorta and inferior vena cava; thus if blood is backed up, the kidneys are quickly affected.
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What are the three major anatomical components of the kidneys?
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Cortex (outer), medulla (inner), and renal pelvis (at hilium).
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Describe the renal cortex.
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Contains all glomeruli, over 85% of nephon tubules reside there, juxtamedullary nephrons.
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Describe the renal medulla.
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Tubules, ducts, Loop of Henle
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Describe the renal pelvis.
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Large collecting area for urine to go to bladder via ureters.
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How many nephrons are in each kidney?
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1 million. 70-80% of glomeruli must be nonfunctioning in order to have signs/Sx that it's damaged.
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Trace a drop of blood through the glomerulus.
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1. Blood enters glomerulus via aorta and renal artery and wide afferent capillary.
2. Glomerulus brings a large surface area of blood capillaries in close contact with Bowman's capsule; the liquid is filtered from blood under pressure (filtration) 3. This filtrate contains water, ions, glucose, salts, minerals, vitamins, some drugs, and urea. 4. The glomerular filtrate enters the proximal convoluted tubule, leaving the capillaries; tubular cells reabsorb 99% of the filtrate components. 5. Protein molecules and RBC are too big to pass into the tubule, thus they continue to travel through the glomeruli through the narrow efferent capillary to the the renal veins and inferior vena cava |
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What about lymph? Where does it go?
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Lymph exit via the hilium and drain into the para-aortic lymph nodes.
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Name the different etiologies of kidney disorders.
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Infection, obstruction, glomerular, congenital, neoplastic.
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What is nephralgia?
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Renal or kidney pain.
nephr/o- = kidney -algia = pain Pain receptors are found in: renal capsule, renal pelvis, and the rest of the urinary tract. CVA tenderness is a clinical manifestation of kidney disease. Affects dermatomes T10, T11, T12, and L1. |
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What can you find in an abnormal urinalysis (UA) test?
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-color, odor, turbidity (cloudy, opaque, or thick with suspended matter like WBC)
-dipstick findings: specific gravity, pH, hematuria, proteinuria, glycosuria, ketones, WBC/leukocyte esterase, and nitrites |
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A urine dipstick finding of decreased specific gravity is associated with what kidney disorder?
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-chronic kidney disease (decreased concentration ability)
-diabetes insipidus |
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A urine dipstick finding of increased specific gravity is associated with what kidney disorder?
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-diabetes mellitus
-SIADS |
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A urine dipstick finding of increased pH (6.5-8.0, alkaline) is associated with what kidney disorder?
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>7.5 UTI with urea-splitting bacteria (e.g., Proteus)
Renal tubular acidosis Calcium or struvite calculi |
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A urine dipstick finding of decreased pH (4.5-5.5, acidic) is associated with what kidney disorder?
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uric acid or cystine calculi
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A urine dipstick finding of hematuria is associated with what kidney disorder?
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-renal cell carcinoma
-tubulointerstitial renal disease -UTI -trauma -glomerulonephritis -obstructive process (e.g., calculi, neoplasms) |
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A urine dipstick finding of proteinuria is associated with what kidney disorder?
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-diabetic nephropathy
-renal hyptertension -glomerulopathies -nephrotic syndrome -renal arteries or venous obstruction |
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A urine dipstick finding of glycosuria or ketones is associated with what kidney disorder?
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-diabetes mellitus
-protein-energy malnutrition |
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A urine dipstick finding of WBC/leukocyte esterase is associated with what kidney disorder?
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UTI
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A urine dipstick finding of nitrites is associated with what kidney disorder?
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UTI (especially with gram-negative bacteria)
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Name some risk factors for UTIs.
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-increasing age
-vesicoureteral reflux (abnormal flow of urine from bladder to upper urinary tract) -congenital anatomic anomalies of the urinary tract -female gender -pregnancy -diaphragms with spermicidal agents for contraception -neurogenic bladder -instrumentation of the urinary tract (catheterization, cystoscopy) -urinary obstruction (calculi, BPH) -glucocorticoids, radiation, or cytotoxic chemotherapy -immunodeficiency conditions such as AIDS -DM -obesity -sickle cell trait |
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What is vesicoureteral reflux?
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Abnormal flow of urine from the bladder to the upper urinary tract; can lead to UTI. There should be a unidirectional flow of urine throughout the urinary tract.
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What is pyelonephritis?
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Infection of the kidney or upper urinary tract infect that affects the renal parenchyma, pelvis, or calices.
Intrarenal infection originate from pH, urea. Postrenal infection orginate from prostatic secretions and glands in women that secrete mucous. The epithelial cells of the nephron tubules trap bacteria for inflammatory mediators to kill the bacteria; leads to pain, urgency, and frequency. |
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Which populations are at risk for kidney disease?
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-premature newborns (underdeveloped glomerulus)
-children (don't know to wipe front to back) -sexually active and pregnant women (all the sex causes trauma, secrete 3-5 mL of mucus daily) -women on certain antibiotics (can wipe out vaginal flora and be vulnerable to opportunistic organisms) -older women (post menopausal women are estrogen-depleted) -diabetics (chronic inflammatory disease, glucose shouldn't be in vascular system, big molecules constantly irritates tubules) -indwelling catheters |
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What is acute pyelonephritis?
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Infection of renal pelvis and interstitium.
-usually unilateral, involving the right kidney in > 50%, 25% involves left kidney, 25% is bilaterial. Very rare to have bilateral kidney disease. |
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What is the etiology of acute pyelonephritis?
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-Pregnancy is a major risk factor due to physical alterations that occur in urinary tract, change in hormones
-DM allows large glucose molecule to circulate and irritate the tubules -vesicoureteral reflux, especially in children (may be a genital malformation, sign is 3+ UTIs in a year) -E. coli in 80% of acute cases Also can be from Proteus mirabilis and Pseudomonas aeruginosa; common from mechanical instrumentation and surgery. These bacterias split urea to ammonia, making an alkaline urine that increases the risk of stone formation. |
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Tell me about the pathophysiology of acute peylonephritis.
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-Ascending bacteria along the ureters may enter via bloodstream
-Delicate, thin epithelial cells trap the bacteria (sticky bomb) for the inflammatory mediators to kill the bacteria -In the meantime, the inflammatory chemokines (leukocytes and inflammatory mediators) leave parenchymal damage to the renal tissue. TEXTBOOK PG 667 Acute infection of the kidney usually originates as an ascending infection but may arrive at the kidney via the bloodstream. Once in the kidney, adhesions on the bacteria bind to epithelial cell receptors, initiating an inflammatory response. Inflammatory chemokines facilitate the movement of WBC into the urine. Inflammatory mediators and bacterial toxins are responsible for the parenchymal damage to the kidney. |
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What are the clinical manifestations of acute peylonephritis?
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-Onset is sudden: pts are acutely ill
-fever, chills, urosepsis (infection due to organisms in the bloodstream originating from the urinary tract) -UTIs: frequency, urgency, dysuria (painful urination) -CVA tenderness Kids will present with fever, elderly will present with slight fever but also change in LOC (due to less robust immune system). Nausea, vomiting, and anorexia are frequent accompaniments, increased the fever-induced dehydration. |
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How do we diagnose acute pyelonephritis?
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UA will present with significant bacteria, RBC, WBC (+casts), nitrites, proteinuria
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What is the treatment for acute pyeloniphritis?
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Patients are treated with antibiotic therapy on an outpatient basis for 7-10 days. If improvement is not noted within 48 hours, a urine culture is obtained and further assessed.
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What is the etiology of chronic pyelonephritis?
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-recurring or inadequately managed infections (Pt takes ABX and stops when s/s stop, but didn't completely wipe out bug. Infection reoccurs.)
-inflammation and scarring of tissue -acute may lead to chronic -often associated with chronic obstruction |
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Which individuals are at risk for chronic pyelonephritis?
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People with obstructive disorders i.e., renal calculi, neurogenic bladder (some type of spinal defect), vesicouretereal reflux, or intrarenal disease
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What are the clinical manifestations of chronic pyelonephritis?
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-may be similar to acute pyelonephritis (fever, chilld, urosepsis, etc.)
-early symptoms are often minimal and may include HTN (because kidneys secrete renin) -progression leads to renal failure |
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How do we diagnose chronic pyelonephritis?
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-ultrasound (US)
-IV pyelogram (IVP) - start IV, inject dye and xray (must be cautious about whether pt will have allergic reaction or renal failure, then dye may become toxic) After IVP, it's common to check for kidney function (urine output, CVA tenderness, and dipstick). |
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What is the treatment for chronic pyelonephritis?
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-remove the obstruction
-give prolonged ABX for infection |
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Name the numerous causes of urinary tract obstruction.
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-congenital
-stones -tumors -trauma -edema -pregnancy -BPH Can develop acutely or slowly. |
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Name the causes specific to intraluminal (within the lumen) obstruction.
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-calculi, clot
-tumor in bladder, kidney, urethra -papillary necrosis |
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Name the causes specific to intraluminal (within the lumen) obstruction.
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-prostatic hypertrophy
-reptroperitoneal fibrosis -tumor in pelvic, retroperitoneal |
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Name the causes specific to acquired obstruction.
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-neurogenic bladder (dysfunction of the urinary bladder due to disease of the CNS)
-ureteral stricture -urethral stricture |
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What is organogenesis?
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Week 1-12 where internal organs are developing, the embryo becomes a fetus.
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What is agenesis?
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Refers to the failure of an organ to develop during embryonic growth and development.
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Name the complications of urinary obstruction.
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-infection
-sepsis -acute renal failure -chronic kidney disease (CKD) -hydroureter -hydronephrosis |
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What is hydroureter?
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Complete obstruction of a ureter results in its dilation.
Abnormal swelling and dilation of the ureter with urine, due to obstruction. |
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What is hydronephrosis?
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Enlarged kidney.
Cystic swelling and dilation of the kidney caused by the accumulation of urine in the renal pelvis as a results of obstruction to outflow. |
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What are the clinical manifestations of urinary tract obstruction?
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-weight gain (from fluid retention)
-nausea -malaise -headache -lower extremity edema *CVA is NOT a presenting sign of urinary tract infection or obstruction. |
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What is renal calculi nephrolithiasis?
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Renal calculi or lithiasis are crystal aggregates composed of organic and inorganic materials located within the urinary tract.
The term renal calculi or nephrolithiasis are used to to describe the formation and passage of calculi anywhere within the urinary tract. |
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Name the different types of nephrolithiasis.
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-calcium oxalate (75%) is the most common
-struvite (7-10%) -uric acid (7-10%) -cystine (1-3%) -ephedrine: guaifenesin, indinavir, xanthine (all <1%) |
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What are the general, broad contributers to renal calculi nephrolithiasis?
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-high pH in urine (alkaline); bacteria split NH3 (ammonia)
-uric acid - gout -prolonged immobilization -purine diets - organ meats -increased BMI |
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What are the risk factors for getting a calcium oxalate nephrolithiasis?
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Risks for this include:
-hypercalcemia (hyperparathyroidism) -hyperuricosuria (excess amount of uric acid in urine) -hyperoxaluria (excess amount of oxalic acid or oxalates in urine) |
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What are the risk factors for getting a struvite nephrolithiasis?
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UTI with urea-splitting bacteria (e.g., Proteus, Klebsiella, Psuedomonas)
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What are the risk factors for getting a calcium oxalate nephrolithiasis?
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-genetic predisposition
-hyperuricosuria associated with gout -acute leukemia -glycogen storage disease -malignancy -excessive intake of meat, fish, poultry -obesity -DM Type 2 -urine pH < 5.5 |
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What are the clinical manifestations of renal calculi nephrolithiasis?
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-presents with acute pain: flank, CVA, testicles or labia
-n/v -hematuria -elevated VS |
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How do we diagnose renal calculi nephrolithiasis?
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-CT
-UA for pH -CBC -BUN/creatinine -dietary history -family history (for passing stow) -other medications (may cause stone or is a diuretic) |
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What is the treatment for renal calculi nephrolithiasis?
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Pain relief, and prevention; may be surgical removal of the stone. US or laser lithotripsy.
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Tell me about glomerular disorders.
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Glomerular disorders result from alterations in the structure and function of the glomerular capillary circulation and are broadly delineated glomerulopathies.
-immune or inflammatory most often implicated |
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What is the classic clinical sign of glomerular disorder?
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Proteinuria
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What are the classifications of degree of proteinuria?
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1. Nephrotic syndrome
2. Nephrosis 3. Nephritic syndrome |
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What is Nephrotic syndrome?
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Protein loss of ≥ 3-3.5 grams/24 hours.
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What is Nephrosis?
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2 grams/day loss of protein
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What is Nephritic syndrome?
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mild proteinuria
*This includes meat eaters (like Cox), runners, and people who have sex a lot. |
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What is ANCA?
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Anti-neutrophil cytoplasmic antibodies
It is a group of antibodies, mainly of the IgG type, against antigens in the cytoplasm of neutrophil granulocytes and monocytes. A patient with this type of inflammation can get glomerulonephritis. |
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What is the etiology of glomerulonephritis?
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Inflammation of the glomerulus and surrounding tissue, related to:
-drugs (alcohol is the biggest drug problem that goes through the kidneys) -toxins -vascular disorder -systemic diseases (DM, HTN) -immunological issues |
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What is the leading cause of chronic and end stage renal failure?
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Glomerulonephritis
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What is the well-known trigger for acute glomerulonephritis?
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Post-streptococcal infection; occurs 7-10 days after infection occurs.
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What is the pediatric etiology for acute glomerulonephritis?
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Group A beta-hemolytic Streptococci
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What are the clinical manifestations of acute glomerulonephritis?
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-hematuria / smoky-colored urine
-edema related to decreased GFR (when assessing, ask pt if they have imprint after removing socks? bra? rings? are their feet too big for their shoes?) -proteinuria -oliguria (scant urine) -HTN -reduced complement levels due to infection |
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Tell me about chronic glomerulonephritis.
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-progressive course of several diseases that lead to chronic renal failure
-several years of proteinuria and hematuria but no other Sx -fibrotic changes with tubular dilation and atrophy may develop |
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Chronic glomerulonephritis associated with what diseases?
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-hypercholesterolemia
-IDDM (DM Type 1) -systemic lupus erythematosus (SLE) - autoimmune disease |
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Describe the general pathology for all of these diseases/disorders.
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They consist of patterns of antigen-antibody complex deposition within the filtration membrane.
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Name the three types of immune mechanism.
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-antigen-antibody
-antibodies against basement membrane -Streptococci release of altering enzyme (remember group A beta-hemolytic streptococci) These all alter membrane permeability and increase swelling, decrease blood flow, and decrease filtration |
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Tell me about the general evaluation and treatment for these diseases/disorder.
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You will see elevated serum creatinine and BUN, proteinuria, hematuria, and casts.
A renal biopsy can truly determine the extent of injury and type. The Tx consists of correcting the underlying cause and controlling for: HTN, edema, hyperkalemia, and hyperlipidemia. |
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In summary, what problems thus are associated when there is renal failure?
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-calcium loss - decreased Ca stimulates PTH; stimulated PTH causes release of calcium from bone and enhance urinary excretion of phosphate,
-anemia - inadequate production of erythropoietin, decreased RBC lifespan less than 120 days -lipids - the ratio of LDL:HDL goes to LDL and an accelerated atherosclerosis occurs -protein loss - proteinuria and a negative nitrogen balance, muscle protein loss -acid base - develops into an acidotic state -hyperkalemia - increased plasma levels with progressive decreased of GFR |
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What is the pathophysiology of renal disease and hypertension?
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-kidneys release renin enzyme in response to the increased pressure in the renal vasculature
-converts Angiotensinogen (go to lungs) to angiotensin I (AI) to angiotensin II (AII) -vasoconstriction and increased arterial pressure -increased aldosterone secretion -systemic hypertension |
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What is the primary medication treatment for HTN from renal disease?
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ACE inhibitors (angiotensin-converting-enzyme inhibitor) that prevents the conversion of AI to AII.
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In order for the kidneys to function properly, what does it require?
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-normal renal blood flow (RBF)
-functioning glomeruli (GFR) -functioning tubules -clearly urinary outflow tract for drainage and elimination of urine formed from body waste |
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What is auto regulation in regards to the renal system?
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It is the maintenance of a her normal intrarenal hemodynamic environment despite changes in the systemic blood pressure. The renal blood flow (RBF), renal plasma flow (RPF), GFR, and filtrate fraction (FF) all work together to regulate and adjust the arterial pressure of the renal artery.
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What is the renal blood flow of the kidneys?
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Renal blood flow (RBF) perfusing the kidneys at 1,200 mL/min.
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What is the renal plasma flow of the kidneys?
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Renal plasma flow (RPF) flowing through kidneys every minute is 50-60% of RBF.
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What is the GFR?
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The GFR is the amount of plasma filtered each minute by the glomeruli; approximately 100-125 mL/min.
*Important to know for post-licensure. |
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What is the FF?
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The filtration fraction (FF) is the ratio of GFR to RBF. Normal is 0.8-0.22.
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What is ARF?
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There is not a precise definition of ARF. It can be classified as the interruption of renal function that has significant ramifications to every body system. Toxins are retained in the body, which can poison every cell in the body (i.e., ammonia).
It's also the sound a dog makes. :) |
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What is the etiology of ARF?
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The comorbidities for ARF includes: pre-existing kidney conditions, HTN, DM, CHF, liver impairment/failure.
In the elderly, the aging kidney is less capable of autoregulating perfusing pressure, has a decreased urine-concentratability, a reduced ability to conserve sodium and diminished response to ADH. Thus, awareness of thirst is decreased, elimination of potassium is decreased, and the GFR of an 80 y/o is half of what it was at 30 y/o. |
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What is the diagnostic criteria for ARF?
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-increase in serum creatinine
-decrease in GFR -oliguria < 400 mL/24 hrs (less than 2 cups/day) -anuria < 100 mL/24 hrs -azotemia: silent, found by changed in BUN -uremia: symptomatic *know these diagnostic terms! -azomtemia / uremia - urea and other toxic wastes in bloodstream, thus stay in body -normal urine output is 1.5-2 L/24 hrs |
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What is the mortality rate of ARF?
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Mortality rate: 7-23%.
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What is pre renal ARF?
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This is when ARF develops the etiology occurs before the kidney itself and the condition decreases perfusion to the kidneys. This happens from actual or relative depletion of circulating blood volume:
-volume depletion = hypotension = hypoperfusion -CHF -hypercalcemia -drug induced (interferes with autoregulation): NSAIDs, COSib, ACEi, ARB (angiotensin receptor blocker), Cyclosproin / Tacrolimus (immunosupressant-anti rejection drug) -Nephrotic syndrome We would worry about someone who just gave birth; there is a huge loss of blood. |
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What is intrarenal ARF?
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This is when ARF develops due to etiology intrinsic to the kidneys. Examples include damage with the blood vasculature, tubules, glomeruli, or interstitium.
Acute tubular necrosis (ATN) is a common cause of ARF, caused by prerenal ischemia. |
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What is ATN?
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Acute tubular necrosis
It's the result of tubular cell injury due to either an ischemic pathology or a toxin; damaged beyond repair. It is the dominant cause of ARF among hospitalized patients in the U.S. Ischemia and inflammation together - ATN may lead to ESCRD (end stage chronic renal disease) |
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What is postrenal ARF?
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This is when ARF develops due to etiology after the kidneys. Examples include obstruction of normal urine flow distal to the kidney. It is most amenable to interventions (we can cure).
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What are the intrinsic etiologies of postrenal ARF?
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Intraluminal: stone, blood clot, papillary necrosis
*papillary = a small, rounded protuberance on a part or organ of the b odd intramural: BPH, ureter stricture, carcinoma prostrate, bladder tumor, radiation fibrosis *intramural = situated within the wall of a hollow organ or cell |
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What are the extrinsic etiologies of post renal ARF?
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-pelvic malignancies
-prolapsed uterus (uterus drops and protrudes through vaginal wall, can pull on ureters) |
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Tell me about the intrarenal autoregulation and what balances out what?
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Vasodilation:
PG, Kinines, ANP, NO Vasoconstriction: Renin, A II, ADH These are overall regulated by RBF and GFR throughout the day. |
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What is ANP?
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Atrial natriuretic peptide
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What is NO?
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Nitric oxide
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What is ESCRD?
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End state chronic renal disease
The kidneys are damaged beyond repair; will need dialysis or transplant. (Although a person can still function with one healthy kidney.) |
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Differ between hypoxia and anoxia.
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hypoxia = decrease in oxygen supply
anoxia = no oxygen supply |
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Name the stages of ATN.
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1. Oliguria
2. Diuretic 3. Recovery |
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Describe the oliguria stage of ATN.
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The urine output drops; leads to hypervolemia, HTN, JVD (jugular vein distention). Metabolic wastes are retained.
Fluid and electrolyte (F&E) imbalance leads to hyperkalemia. Remember, hyperkalemia affects body. Every cell has a sodium-potassium pump, can lead to seizures, etc. Uremic syndrome: interferes with CNS, peripheral nervous system, cardiovascular system, immune system, GI system, skin, and acid-base balance. (Pg. 689, table 28-3) |
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Describe the diuretic stage of ATN.
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Polyuria concentrating mechanism has not recovered (pt still peeing a lot; may pee up to 4-5 L/day); leads to fluid volume deficit.
Elevated BUN continues. F&E imbalance: hypokalemia. |
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Describe the recovery state of ATN.
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Full recovery of renal function. Serum creatinine is normalized.
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Discuss the association of chronic kidney disease (CKD) and anemia.
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Anemia is a common complication of chronic kidney disease (CKD) because the kidneys are unable to manufacture enough erythropoietin, a hormone that regulates the production of RBC.
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