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NURS 350 Patho renal
Pathophys - kidney, renal alterations
| Question | Answer |
|---|---|
| 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
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