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NURS 350 Patho renal

Pathophys - kidney, renal alterations

QuestionAnswer
kidney hormones renin (BP), EPO (RBCs), Vit D3 (to absorb Ca++ in renal tubules), ANH (atrial natiuretic hormone, sometimes ANF for factor)
What 3 layers to glomerlular filtrate pass through inner capillary endothelium, shared basement membrane, outer epithelium. Bmem has anionic proteins to prevent filtration of plasma proteins
what % of CO does kidney receive 20-25% which means 1000 ml of blood per minute
from renal plasma flow, what percentage is filtered at glomerulus to pass into Bowmans 20% of renal plasma flow is filtered, which is 130 ml per minute
what is GFR filtration of plasma per unit time - 120 ml per minute - 99% of filtrate is reabsorbed. most commonly measured by creatinine
GFR is directly related to RBF which is regulated in 3 ways RBF regulated by intrinsic autoregulatory, neural and hormonal
renal blood flow is autoregulated between a range of perfusion pressures - which means local mechanisms keep rate of RBF and GFR at constant arterial pressures between 80 - 180 mmHg. local mechanisms prevent wide arterial pressure fluctuations from being transmitted to glomerular capillaries
what is the effect of DECLINING arterial pressure on RBF stretch on afferent arterial wall decreases -->arterial relaxes--> RBF INCREASES
what is the effect of INCREASING arteriolar pressure on RBF stretch on afferent wall increases--> arteriole contracts --> RBF decreases
High BP is to decreased RBF as . . . low BP is to increased RBF
sympathetic NS cause vasocon to decrease RBF, as does exercise, hypoxia and body position. how dose body compensate when symp activity --> vasoCON, RBF/GFR are decreased. This REDUCES excretion of Na/H20, which are retained to increase blood volume and increase pressure
severe hemorrhage and RBF severe bleed causes symp stim --> intense vasocon --> decreased RBF/GFR
What is clearance indirect measure of GFR, tubular secretion, reabsorption and RBF. GFR is BEST estimate as to functioning renal tissue
if we have a decrease in GFR what does this indicate that we have a corresponding loss/damage to nephron
three markers to test for clearance inulin, creatine, cystatin C
how do we measure creatine clearance 24 hour urine collection and a serum Pcr
what is normal Pcr 0.6 - 1.5 mg/dl
what does elevated Pcr indicate indicates a decrease in GFR (less creatine being filtered to urine, more to blood)
can we use creatine clearance for crush, trauma or muscle damaged patients no, because creatine is made by muscles and released at consistent rate. must use Cystatin C as a marker for these patient
What does BUN = blood urea nitrogen measure reflects the GFR and urine-concentrating ability.
normal BUN 8-25 mg/dl
what does an elevated BUN indicate that GFR is low, less urea filtered by kidney, less being excreted, more urea in blood
where in kidney is urea reabsorbed urea reabsorbed through permeable tubules, affecting ability to concentrate urine
Increased BUN associated with these disease states increased BUN associated with dehydration, acute/chronic RF when passage of fluid throughtubules is slowed
what metablolic conditions are also indicated by abnormal BUN BUN associated with changes in altered protein intake and protein catabolism
profile of normal UA pH 4.6 - 8.0, no blood cells except a few casts, SG = 1.02, negative for bilirubin, urobilinogen,ketones and glucose.
electrolyte values of normal UA Na = 100-260, K= 25-100
Normal values of Pcr and BUN Pcr = 0.6 - 1.5 BUN = 8-25
oliguria diminished urine < 400 ml/day
where can a urinary tract obstruction occur ANYWHERE along urinary tract (kidney, bladder, ureters, urethra)
common causes of congenital or acquired obstructions tumors, calculi, pg, trauma, prostatic hypertrophy, loss of urethral peristalsis, loss of bladder muscle function
Four main categories of urinary tract obstruction 1-obstructive 2- infectious 3- injurious 4- failure
Acute, complete obstruction accumulation of urine behind obstruction --> retrograde increase in hydrostatic pressure --> decreased GFR (can go do zero)
Chronic, partial obstruction compression/atrophy of kidney structures with tubular damage
MOA of chronic, partial obstruction tubular damage results in DECREASED ability to conserve Na/H20 . . inability to excrete H+/K+
if chemistry labs came back low Na, High K, High H+ . . .this would indicate would indicate chronic, partial obstruction
common causes of obstruction neurogenic (overstimulated) bladder, renal tumors, bladder tumors
how do we treat obstruction, what to watch for treatment to relieve obstruction. followed by massive diuresis (as high as 10L per day). watch for dehydration and excessive Na loss
what are complications of obstruction? infection and renal failure are complicatons
what is most common cause of upper urinary obstruction nephrolithiases (renal calculi)
What most often contributes to lower urinary tract obstructions generally confined to alterations in urination patterns (increased frequency, poor force of stream, urgency with hesitancy, incomplete bladder emptying, urinary retention)
75% of all renal calculi are composed of calcium oxylate and calcium phosphate
other sources of calculi Mg, NH4-PO4, urice acid, cystine
contributing factors of renal calculi high concentration of minerals, correct pH (alkaline urine favors Ca++ stones). decreased nephrocalcin, dehydration. Also diet, drugs and diseases such as gout/uric acid
how does calculi form forms around a nidus, becomes trapped and accumulates other crystals
where do calculi appear they appear in renal tubules, calcyes, pelvis, ureters, bladder
clinical manifestations of calculi pain (renal colic flank/groin), n/v, hematuria, bacteriuria
treatment of calculi deal with pain first, then stone passage, prevent new stones
s/s cystitis (bladder inf/UTI) frequency/urgency/dysuria --- suprapubic/flank/low pack pain --- hematuria, cloudy urine ---10% asymptomatic/30% no bacteria in urine
UTI definition infection of any structure in urinary tract - caused by baceteria
C & S will be positive UTI if these bacteria present Gram - E.Coli, Proteus, Pseudomonas.
less common microbes in UTI staphylococcus, candida/fungi in immunosuppressed
what is cystitis inflammation of bladder due to UTI.
how is bladder mucosa altered from cystitis Mild infl = hyperemia mod/adv = hemorrhage/pus formation most severe = necrosis of bladder wall chronic = sloughing and ulceration
What is pyelonephritis differs from simple UTI as it occurs proximal to bladder in ureters, or renal pelvis/interstitium.
How does pyelonephritis present presents either unilateral or bilateral, more common in woman with same G- bugs - primarily E.Coli (proteus, pseudomonas)
what are risk factors for acute pyelonephritis renal calculi, vesicourethral reflux (urine backs up bringing bacteria), pg, neurogenic baldder, instrumentation, sexual trauma
do we find acute pyelonephritis in the glomeruli no, only kidney (tubules, pelvis, calyces, medulla) and book says in ureters
pathophys of pyelonephritis infection --> inflamm process that is FOCAL AND IRREGULAR --> medulla infiltrated with WBCs (glomeruli not effected)--> purulent urine/abcess/necrosis
acute pyelonephritis - bacterial count and does it cause renal failure bacteria count decreases until urine is sterile, rarely causes renal failaur
clinical manifistations - treat with Antibiotics - of acute pyelonephritis fever/chills. flank/groin pain. frequency/dysuria. costovertebral tenderness. children/elderly show nonspecific fever, malaise
causes of chronic pyelonephritis caused by persistent/recurrent autoimmune process, NSAIDs, ischemia, radiation. Also may due to calculi or ureteral reflux
does chronic pyelonphritic lead to renal failure yes, Yes, YES it CAN lead to renal faire!
pathophys of chronic pyelonephritis chronic obstruction/inf/inflamm --> atrophy in renal pelvis/calyces --> tubules destroyed --> can't concentrate urine -->chronic renal failure
clinical manifestations of pyelonephritis can't conserve Na yet HTN, hyperkalemia, metab acidosis, dehydration/dilute urine. frequency/dysuria/flank pain
When does fever present - lower UTI or pyelonephritis fever presents with pyelonephritis
glomerulonephritis is inflamm of glomerulus caused by caused by immunologic abnormalities, drugs, toxins, ROS, vascular disorders, systemic diseases
what is MOST COMMON CAUSE of chronic and end-stage renal failure glomerulonephritis is most common cause
what is most common cause of glomerulonephritis throat/skin infections (b hemolytic stretpococcus)- - - followed by bacterial endocditis (strep/staph) and viral diseases (varicella/HepB/C and HIV)
pathophys of glomerulonephritis immune complexes deposit in glomerulus ---activate phages/complement/Tcell/ROS ---damage to glomerular epi---platelet aggregation/glomerular sclerosis---decreased glomerular blood flow
clinical manifestations of glomerulonephritis hematuria/RBC casts---protenuria---DECREASED GFR---oliguria---ECF edema---HTN
define renal insufficiency down to 25% of normal GFR (25/30 ml/min)
define renal failure GFR decreased to 10-25% of normal
define ESRF end-stage renal failure less than 10% of renal function remains
what type of renal failure is evidenced by increase in BUN, Pcr and oliguria acute renal failure evidenced - abrupt drop in renal function, usually reversible
What is acute prerenal failure not enough blood going to glomerulus --> decreased GFR --> acute tubular necrosis or cortical necrosis
Acute renal failure pt presents with hyperkalemia. one treatment? pt can't excrete K,so we can admin glucose/insulin (cuz glucose/insulin takes K with it into the cells)
what causes decreased renal blood flow/poor perfusion seen in prerenal acute RF vasocon, hypoTN, hypovolemia, hemorrhage, inadequate CO
what is most common type of renal failure intrarenal RF is most common type, affects the kidney itself
What causes intrarenal acute RF ATN = acute tubular necrosis bwo ischemia/ROS --cellular injury/swelling/necrosis.
kidney/nephron surgery, nephrotoxic drugs, xray media associated with what type of RF associated with intrarenal acute RF
TN or ATN (tubular necrosis) generally associated with this underlying condition usually associated with ischemia
what is postrenal acute RF usually occurs after kidney bwo urinary tract obstruction & edema of tubular lumen - - - affects kidneys bilaterally
manifestations of postrenal acute RF hours of anuria - flank pain - polyuria.
pts DO recover from ACUTE renal failure by these clinic progressions oliguria - diuresis -recovery to normal function
do pts recover from CHRONIC renal failure no, these patients have progressive IRREVERSIBLE loss of renal function. the manifestations are described in terms of UREMIA or uremic symtoms
what are the UREMIC/UREMIA symptoms seen in chronic renal failure anorexia/wt loss --- n/v/d/c ---itching---edema---neuro changes
what is state of kidney when it exhibits uremia didneys can adapt until <25% (renal insufficiency) - once function falls below 25% they go into failure
lab/diagnostic indicators of chronic RF high Pcr, high BUN, small kidney size, biopsy confirms diagnosis
how do we manage end-stage RF dialysis is a bridge to kidney transplant. diet needs restrictions in pro/K+. Obsever Na/H20. EPO needed for RBCs. control BS if related to DM
pts with chronic renal failure have liver AND kidney problems --> coagulation problems --> prolonged coagulation bwo platelet dysfunction at vascular endothelial junction
what is azotemia bnormally high levels of nitrogen-containing compounds, such as urea, creatinine, various body waste, etc. generally found in all renal failures
Created by: lorrelaws