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ANP
- Dilates the afferent arterial and constricts the efferent arterial
- decreases renin secretion
- inhibits the epithelial Na channel in the DCT
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In diabetic patients
The high osmolarity caused by glucose concentration increases thirst
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Two affects of loop diuretics
- increase the amount of solutes delivered to the distal tubules which decrease water lost
- disrupt the counter current multiplier
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Thiazides
- block the Na Cl co transporter in the distal tubules
- Chlorothiazide
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Acetazolamide
- carbonic anhydrase inhibitor
- proximal tubule
- blocks Na reabsorption through the Na H counter transport, No H to exchange
- Cause a degree of acidosis
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Aldosterone inhibitors
- spironolactone and eplerenone
- inhibit the Na K pump in the collecting tubules
- the Na then acts like an osmotic diuretic
- K is sparring and aldosterone inhibitors also move K from intercellular to extralcellular
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Na channel blocker diuretics
- amiloride and triampterene
- inhibit Na absorption and K secretion in the collecting tubules
- differ from aldosterone inhibitors by directly blocking the Na absorption on the luminal side
- This decrease in intercellular Na stops the action of the basil membrane Na K pump
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Three main categories of acute renal failure
- decreased blood supply. PreRenal condition. Hemorrhage, cardiac failure, low blood pressure
- Intrarenal
- Postrenal. obstruction of the urinary collecting system. Kidney stones of calcium, irate and cystine
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Main purpose of high blood flow to kidneys
- provide enough plasma for the high rates of glomerular filtration needed for effective regulation of body fluid and solute concentration
- Decreased blood flow is accompanied by decreases GFR and decreased output of salt and water
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Oliguria
decreased urine production below the intake of salt and water
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Anuria
total cessation of urine production
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Renal failure may be reversed
- as long as blood flow does not fall below 20-25%
- basil requirement of the renal tubule cells with no ATP pumps functioning
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Why can the kidney survive so long with diminished blood flow
- when blood flow is reduced the GFR is reduced
- The decrease in GFR reduces the amount of Na and Cl filtered and in turn reduces the amount that must be reabsorbed
- This reduced reabsorption decreases the amount of oxygen needed for metabolism by the kidney
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Intra renal acute failure
- conditions that injure the glomerular capillaries or other vessels
- conditions that cause damage to the renal interstitial
- conditions that damage the renal tubule epithelium
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Causes of prerenal failure
- volume depletion; hemorrhage, diarrhea or vomiting, burns
- cardiac failure; MI, valvular damage
- vasodilation and hypotension; anaphylactic shock, anestesia, sepsis and infection
- primary renal artery; stenosis or embolism
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causes of internal renal failure
- small vessel and glomerular injury; vasculitis, cholesterol emboli, malignant hypertension,
- Tubular epithelia injury (tubular necrosis); ischemia, heavy metal toxicity
- renal interstitial injury; pyelonephritis, allergic nephritis
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Acute glomerulonephritis
- type of intrarenal failure
- usually caused by abnormal immune reaction
- group A hemolytic beta streptococci
- The immune complex gets trapped in the glomerulus
- This tapping causes mesanchial cells to proliferate, many pores become blocked and the unblocked pores become excessively permeable
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Tubular necrosis
- intrarenal failure
- severe ischemia and poisons toxins and medication
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Tubular necrosis cased by ischemia
- circulatory shock or other disturbances of blood flow
- necrotic tubule cells slough off and plug the nephrons, the affected nephrons fail to excrete urine even after blood flow is returned if the plug is still there
- The most common causes of ischemia are the prerenal causes associated with shock; hemorrhage, anesthetics, diureha, burnes ext
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Toxins that can cause acute renal failure
- carbon tetrachloride
- heavy metals; mercury and lead
- insecticides
- medications; tetracyclins
- cancer drugs
- cause cells to slough off and plug nephrons
- If glomerular membrane is intact cells can regenerate in 10-20 days
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Blockage of urine excretion, post renal
- if output from one kidney is blocked fluid volume will not change significantly
- contralateral kidney will increase in size and urine production
- chronic obstruction lasting more then several hours can lead to kidney failure
- stones, bladder obstructions, urethra damage
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Physiology of acute renal failure
- retention of water, waste products of metabolism, and electrolytes
- can lead to edema and HTN
- Retention of K is a large problem, develop hyperkalemia. Decreases the membrane potential which leads to a decreased AP
- Also develop acidosis
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Chronic renal failure
- results from the progressive and irreversible loss of large numbers of functioning nephrons
- clinical symptoms occur when you lose around 70-75%
- can occur from disorders in the blood vessels, glomeruli, tubules interstitial, lower urinary tract
- end result is always the same, decrees in functional nephrons
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causes of chronic renal failure
- metabolic disorders; DM, obesity, amyloidosis
- HTN
- Renal vascular disorders; atherosclerosis
- Immune
- Infection; pylonephritis, TB
- primary tubular disorders; toxins
- Urinary tract obstruction
- Congenital; polycystic disease
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Adaptive change after loss of kidney mass
- the functional kidney mass will hypertrophy and compensate for the loss of tissue
- over a period of years the renal functional changes may lead to further injury of the remaining nephrons, mostly the glomeruli
- There is a chronic increase in pressure and stretch of the small arterioles believed to cause sclerosis
- This cycle of compensation and damage becomes vicous and leads to end stage disease
- Only way to slow it down is to lower renal blood pressure, ACE inhibitrs
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Important risk factors for end stage renal disease
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Vascular lesions that can lead to renal ischemia
- atheroslerosis; large renal arteries with progressive sclerotic constriction. Usually affects one kidney more then the other
- fibromuscular hyperplasia;
- nephrosclerosis; sclerosis of small arterioles
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Benign nephrosclerosis
- seen in 70% of people over age 60
- occurs in small interlobular arteries and in afferent arterioles
- begins with leakage of plasma through the endothelium, This causes fibrinoid deposits to develop in the medial layer followed by thickening of the vessel wall
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Glomeruloscerosis
- sclerosis of the glomeruli
- increqased frequency in DM and HTN
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Strptococcal infection glomerulinephtits
- Strep infection is the leading cause of acute
- chronic is lupus
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chronic glomerulonephritis
- results from the accumulation of antibody-antigen complex in the glomerular membrane
- causes inflammation, progressive thickening of membranes, eventual invasion of glomeruli by fibrous tissue
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Clinical conditions of the bladder that can lead to pylonephritis
- pylonephritis; bacterial infection of the renal interstitial tissue
- inability of the bladder to empty completely
- obstruction in urinary outflow
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Cystitus
inflammation of the bladder
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Vesicoureteral reflux
urine is propelled up the ureters during matriculation
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Patients with pyelonephritis
- infection usually affects the medulla more then cortex
- can not concentrate urine ; loss of counter-current multiplier
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Creatinine filtration rate
GFR x plasma concentration
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Isosthenuria
inability of the kidney to concentrate urine
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Ability to concentrate urine with lose of nephrons
- the rapid flow of fluid through the collecting ducts prevents water reapsoption
- the rapid flow through the loop of henle and collecting ducts prevents counter current from operating properly
- As more nephrons are destroyed the healthy ones compensate more by increasing there GFR and causing the above to loses in concentration
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Important clinical renal function test
test the ability off the kidney to concentrate urine when water is restricted for 12 hours
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You can remove a kidney in renal hypertension
if one kidney is ischemic and is the source of excess renin it can be removed
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Azotemia
- increase in non protein nitrogen
- urea, uric acid, creatinine
- End produces of protein metabolism
- measuring plasma concentrations gives a good indicator of renal disease
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Anemia in chronic renal failure
decrease in erythropoietin secretion
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Osteomalacia in chronic renal failure
- bones are partially degraded
- serous damage to the kidney reduces the kidneys ability to generate the active form of vit D3
- Also a rise in serum phosphate levels binds with calcium in the blood so ionized calcium falls stimulating parathyroid hormone release
- secondary hyperparathyroidism causes a release of calcium from the bones
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Angiotension 2
increases GFR but increases reabsorption more. Increase in Na reabsorption in the proximal tubules and a lower pressure in the vasa recta so less hydrostatic pressure leads to increased water absorption and increases plasma fluid and pressure
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Non hypertensive renal failure
with loss of large numbers of nephrons but no release of renin from ischemia
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Normal plasma glucose but glucose in the urine
renal glycosuria
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Aminoacidurea
- failure to reabsorb amino acids
- essential cystienurea; leads to kidney stones
- simple glycineurea
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Rickets that is refractory to Vit D therapy
- hypophosphatemia
- renal inability to absorbe phosphate
- so signs at first but after a while lose the ability to calcify bone
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Two types of diabetes insipidus
- nephrogenic; inability of the kidneys to respond to ADH
- nerogenic; inability of the hypothalamus to produce ADH
- Person must drink large amounts of water
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Faconi's syndrome
- increased urinary excretion of all amino acids, glucose, and phosphate
- can also have failure to reabsorb bicarb
- increased excretion of K and Ca
- nephrogenic diabetes insipidus
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Causes of faconi's syndrome
- heriditary defect in transport proteins
- toxins or drugs
- ischemic injury
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Rate of movement during dialysis depends on
- solute concentration gradient; greatest transfer is at the beginning when gradient is the largest
- rate of flow
- surface area
- permiability
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