Upgrade to remove ads
Only $35.99/year

Renal Functions and Disorders

Terms in this set (85)

Volume is regulated by monitoring and adjusting
Na content
Osmolality is regulated by monitoring and adjusting
H2O content, specifically ECV
What causes thirst
increase plasma osmolarity, dry mouth/throat, decrease plasma volume
What leads to an increase in renin secretion
decreased stretch of granular cells, decreased rate of fluid delivery to macula densa, increased activity in renal sympathetic nerves
what causes an increase in aldosterone secretion
increased ACTH release from anterior pituitary, increased plasma K+ conc., in increase in plasma angiotensin II due to renin
increased activity of the SNS will...
result in an increase in afferent arteriole resistance due to vasoconstriction-decrease GFR, stimulate renin release, increase reabsorption of Na+ in the PT
ADH, RAAS, Thirst, and SNS will be activated when
volume is decreased
ANP will be activated when
volume is increase
ADH and Thirst will be activated when
osmolarity is increased
quantitative test of renal function
clearance and GFR, clearance and RBF, blood tests for creatinine and urea as well as glucose, urinalysis such as pH and specific gravity
qualtitative test of renal function
presence of cells, casts, crystals and bacteria in the urine
Clearance
the rate at which a substance can be cleared from the blood by the kidneys
when GFR declines there will be a ____ in plasma creatinine
increase
True or False: plasma creatinine is valuable for monitoring chronic and acute renal disaease
False. Only valuable for monitoring chronic
Blood urea nitrogen (BUN) reflects
glomerular function and urine concentrating ability
when GFR drops BUN will
rise
dehydration, acute renal failure, chronic renal failure will cause BUN to
increase
various problems of renal disease
acid-base and electrolyte disturbance, inability to concentrate urine as well as anuria, oliguria, polyuria, decreased EPO synthesis, hematuria, azotemia, proteinuria
type of defect that occurs to the ureter in congenital urinary tract obstruction
various types of obstruction
type of defect that occurs to the bladder outlet in congenital urinary tract obstruction
bladder neck obstruction
type of defect that occurs to the urethra in congenital urinary tract obstruction
stricture
cause of urinary tract obstruction to the ureter in acquired intrinsic
calculi, uric acid crystals
cause of urinary tract obstruction to the bladder outlet in acquired intrinsic
benign prostatic hyperplasia, calculi, diabetic neuropathy
cause of urinary tract obstruction to the urethra in acquired intrinsic
calculi
cause of urinary tract obstruction to the ureter in acquired extrinsic
pregnant uterus, retroperitoneal fibrosis, carcinoma
cause of urinary tract obstruction to the bladder outlet in acquired extrinsic
carcinoma, trauma
cause of urinary tract obstruction to the urethra in acquired extrinsic
trauma
three major types of kidney stones
calcium oxalate, struvite, uric acid
contributing factors to stone development
high urine concentration of stone-forming substances, urine pH that affects substance solubility, low urine output, tubular defects, facilitators and inhibitors of growth, various diseases, drugs, diet
what is the hallmark symptom of kidney stones
pain
can see a decrease in GFR due to
reduced glomerular hydrostatic pressure such as with circulatory shock; increased bowmans capsule hydrostatic pressure due to an obstruction; increased plasma colloid osmotic pressure such as in liver disease, reduced permeability of the glomerular capillaries sucha s in diffuse glomerular disease; loss of filtration surface as see in progressive renal failure
creatinine excretion depends largely on filtration so relatively small decreases in GFR result in
significant elevations in plasma creatinine
substances such as K+ and H+ are filtered and secreted and therefore significant decreases in GFR ...
must occur before there are alterations in the plasma concentrations of K+ and H+
Na+ is so thoroughly regulated that...
GFR has to drop to almost 0 before plasma concentration of Na are adversely affected
What is the primary cause of glomerular disease
immunologic mechanisms
what is the most common cause of chronic and end-stage renal failure
glomerular diseases
nephrotic sediment
massive proteinuria and no hematuria
nephritic sediment
minimal proteinuria and hematuria
chronic glomerular sediment
less proteinuria and hematuria, has waxy casts, granular casts
Determinants of severity of glomerular injury
nature of insult and mediators involved; site of injury with the glomerulus; speed of onset, extent, and intensity of disease
factors that cause inflammation in glomerulonephritis
immunologic-most frequent; drugs or toxins; vascular disorders, systemic diseases
acute glomerulonephritis
abrupt onset(usually 7-20 days after strep throat or skin infection); common in children; dcrease GFR due to thickening of glomerular membrane following immune response; more severe disease can be seen if prolonged infection before antibiotic treatment; most recover without significant loss of renal function
IgA nephropathy
most common form of nephroritis-cause unknown; usually after upper respiratory or GI viral infection; proliferation of mesangial cells; release of oxidants and proteases causing glomerular injury; 50% progress to renal failure
rapidly progressive glomerulonephritis (RPGN)
idiopathic or associated with number of other glomerular diseases; goodpasture syndrome is a form of RPGN-antibodies form again pulmonary and glomerular capillary basement membranes; extensive proliferation of cells into Bowmans space; progresses to renal failure in weeks
chronic glomerulonephritis
encompasses several glomerular diseases leading to chronic renal failure; proliferation of mesangial cells-focal or diffuse; tubular dilation and atrophy may develop; primary cause difficult to determine in most cases; diabetes and SLE are secondary causes
General clinical manifestations of glomerulonephritis
hematuria with RBC casts and proteinuria exceeding 3-5g/da (nephrotic syndrome; albumin is primary protein); fluid retention due to reduced GFR and salt/water reabsorption leading to volume expansion and hypertension
hematuria
characterized by smoky brown-tinged urine with cell casts
nephrotic syndrome
excretion of 3.5g or more of protein (primarily amlbumin) in the urine per day. Additional findings incluse hypoalbuminemia, edema, hyperlipidemia, and lipiduria. Minimal change disease, membranous glomerulonephritis and focal glomerulosclerosis are directed related to nephrotic syndrome
medullary cystic disease
salt wasting
Liddle's and Bartter's syndromes
hypokalemia
diabetes insipidus
concentrating defect
renal tubular acidosis, type I
impaired or reduced proton secretion
renal tubular acidosis, type II
bicarbonate reabsorption
X-linked hypophosphatemia
phosphate reabsorption
Faconi Syndrome
reduced reabsorption of glucose and amino acids
vitamin dependent rickets type I
defective renal production of vitamin D
vitamin dependent rickets type II
defective renal resistance to vitamin D
renal insufficiency
decline in renal function to about 25% of normal GFR
kidney injury
further significant reduction in renal function
end-stage renal disese (ESRD)
less than 10% of renal function remains
acute
abrupt decline and rapidly progressive; can be reversible
chronic
progressive over years and leading to ESRD
Azotemia
increased serum levels of urea and creatinine
uremia
a syndrome characterized by azotemia and accompanied by fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes due to accumulation of toxic wastes, electrolyte disorders and deficiency states
acute kidney injury (ARF, AKD, AKI)
abrupt reduction in renal function associated with oliguria (<400 ml/day), elevated BUN and creatinine as well as acid-base disturbances
possible causes of prerenal acute renal failure
due to impaired renal blood flow -most common cause; can result from renal vasoconstriction causing hypovolemia, hypotension, hypoperfusion, or decreased cardiac output;
possible causes of intrarenal acute renal failure
acute tubular necrosis
possible causes of postrenal acute renal failure
obstructive uropathies (usually bilateral)
prerenal acute renal failure
most common cause of acute renal failure; due to impaired renal blood blow; usually kidney tissue is not damaged, however, acute tubular necrosis can eventually occur if blood volume or pressure are not restored; will see activation of regulatory mechanisms that increase salt and water reabsorption since the kidney is sensing a decrease in blood flow; this will be helpful by maintaining some level of perfusion to the kidney; also see increased synthesis of PG's that cause preferential dilation of the afferent arteriole and angiotensin II which vasoconstricts the efferent arteriole; drugs which block PG and angiotensin II synthesis can have significant effects on the compensatory regulatory mechanisms in compromised individuals
Intrarenal acute renal failure
Results from DIRECT damage to the kidney itself. Acute tubular necrosis (ATN) is the most common cause-postischemic or nephrotoxic. Ischemic or nephrotoxic causes both result in tubular injury leading to loss of urine-concentrating ability, defective distal Na reabsorption as well as a possible reduction in GFR; ultimately see oliguria.
Postischemic ATN
Relates to intrarenal acute renal failure. ATN caused by ischemia typically occurs after surgeries, but can be associated with a number of other conditions such as sepsis, burns, and trauma. Ischemia generateds oxygen free radicals and inflammatory mediators causing cell swelling, injury, and necrosis.
Nephrotoxic ATN
Relates to intrarenal acute renal failure. Nephrotoxic ATN produced primarily by aminoglycoside antibiotics (and others); these drugs have two effects: 1) they bind to the tubular epithelial cells and cause changes in the cell membrane; 2) they are transported into the cells and enter lysosomes causing release of lysosomal enzymes
Postrenal acute renal failure
rare in occurrence and is due to urinary tract obstructions
what are the 3 phases of clinical progression of acute renal failure
1) oliguria (decrease in urine output); anuria is uncommon in ATN; anuria usually suggests bilateral renal artery occlusion, obstructive uropathy, or acute necrosis. 2) diuresis 3) recovery
Clues for diagnosing prerenal acute renal failure
symptoms of thirst; orthostatic dizziness as well as physical evidence of orthostatic hypotension and tachycardia; decreased skin turgor and dry mucos membranes; progressive fall in urine output and treatment with NSAIDs and ACE inhibitors
Clues for diagnosing intrarenal acute renal failure
Due to ischemia: severe hypoperfusion following shock or surgery; likelihood of ischemic ARF is increased if it persists following normalization of systemic hemodynamics.
Due to nephrotoxic: may be evident based on drug history of patient (antibiotics)
Clues for diagnosing postrenal acute renal failure
will present with suprapubic and/or flank pain due to urine outflow obstruction; history of prostate disease or drugs that may affect micturition
chronic kidney disease
Progressive, irreversible loss of renal function affects numerous important regulatory processes of the kidney. Essentially every organ system will become affected. Most individuals will progress to ESRD.
Symptoms of chronic kidney disease
increased plasma BUN, creatinine and K as well as alterations in salt water balance do not become evident until renal function declines to less than 25% of normal
3 most common causes of chronic kidney disease
diabetes, hypertension and primary glomerulonephritis
pathophysiology of chronic kidney disease
changes that occur are somewhat LOCATION specific. tubular damage results in renal tubular acidosis, salt wasting and difficulty in diluting or concentrating urine; vascular or glomerular damage results in proteinuria, hematuria and nephrotic syndrome
what is the clinical manifestation of chronic kidney disease
uremia
GFR's for Mild, Moderate, and Severe CKD
Mild CKD= GFR of 60-90 ml/min
Moderate CKD= GFR of 30-59 ml/min
Sever CKD= GFR of 15-29 ml/min
ESRD=GFR of below 15 ml/min
pathophysiology of end stage renal disease
signs and symptoms due to uremia-elevations in blood concentrations of toxins as well as other organic compounds. Ultimately see affects on all organ systems
clinical manifestations of end stage renal disease
impaired salt and water balance leading to volume expansion and hypertension as well as edema (particularly in the lungs); impaired ability to dilute and concentrate the urine; hyperkalemia leading to cardiac arrhythmias; metabolic acidosis; renal osteodystrophy and second hyperparathyroidism, hyperphosphatemia; anemia due to insufficiency of EPO synthesis; bleeding events; hyperlipidemias
Other sets by this creator