Pathophys - kidney, renal alterations
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| kidney hormones | renin (BP), EPO (RBCs), Vit D3 (to absorb Ca++ in renal tubules), ANH (atrial natiuretic hormone, sometimes ANF for factor)
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| 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
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| what % of CO does kidney receive | 20-25% which means 1000 ml of blood per minute
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| 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
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| what is GFR | filtration of plasma per unit time - 120 ml per minute - 99% of filtrate is reabsorbed. most commonly measured by creatinine
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| GFR is directly related to RBF which is regulated in 3 ways | RBF regulated by intrinsic autoregulatory, neural and hormonal
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| 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
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| what is the effect of DECLINING arterial pressure on RBF | stretch on afferent arterial wall decreases -->arterial relaxes--> RBF INCREASES
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| what is the effect of INCREASING arteriolar pressure on RBF | stretch on afferent wall increases--> arteriole contracts --> RBF decreases
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| High BP is to decreased RBF as . . . | low BP is to increased RBF
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| 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
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| severe hemorrhage and RBF | severe bleed causes symp stim --> intense vasocon --> decreased RBF/GFR
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| What is clearance | indirect measure of GFR, tubular secretion, reabsorption and RBF. GFR is BEST estimate as to functioning renal tissue
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| if we have a decrease in GFR what does this indicate | that we have a corresponding loss/damage to nephron
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| three markers to test for clearance | inulin, creatine, cystatin C
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| how do we measure creatine clearance | 24 hour urine collection and a serum Pcr
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| what is normal Pcr | 0.6 - 1.5 mg/dl
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| what does elevated Pcr indicate | indicates a decrease in GFR (less creatine being filtered to urine, more to blood)
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| 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
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| What does BUN = blood urea nitrogen measure | reflects the GFR and urine-concentrating ability.
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| normal BUN | 8-25 mg/dl
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| what does an elevated BUN indicate | that GFR is low, less urea filtered by kidney, less being excreted, more urea in blood
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| where in kidney is urea reabsorbed | urea reabsorbed through permeable tubules, affecting ability to concentrate urine
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| Increased BUN associated with these disease states | increased BUN associated with dehydration, acute/chronic RF when passage of fluid throughtubules is slowed
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| what metablolic conditions are also indicated by abnormal BUN | BUN associated with changes in altered protein intake and protein catabolism
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| 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.
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| electrolyte values of normal UA | Na = 100-260, K= 25-100
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| Normal values of Pcr and BUN | Pcr = 0.6 - 1.5
BUN = 8-25
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| oliguria | diminished urine < 400 ml/day
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| where can a urinary tract obstruction occur | ANYWHERE along urinary tract (kidney, bladder, ureters, urethra)
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| common causes of congenital or acquired obstructions | tumors, calculi, pg, trauma, prostatic hypertrophy, loss of urethral peristalsis, loss of bladder muscle function
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| Four main categories of urinary tract obstruction | 1-obstructive
2- infectious
3- injurious
4- failure
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| Acute, complete obstruction | accumulation of urine behind obstruction --> retrograde increase in hydrostatic pressure --> decreased GFR (can go do zero)
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| Chronic, partial obstruction | compression/atrophy of kidney structures with tubular damage
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| MOA of chronic, partial obstruction | tubular damage results in DECREASED ability to conserve Na/H20 . . inability to excrete H+/K+
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| if chemistry labs came back low Na, High K, High H+ . . .this would indicate | would indicate chronic, partial obstruction
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| common causes of obstruction | neurogenic (overstimulated) bladder, renal tumors, bladder tumors
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| 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
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| what are complications of obstruction? | infection and renal failure are complicatons
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| what is most common cause of upper urinary obstruction | nephrolithiases (renal calculi)
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| 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)
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| 75% of all renal calculi are composed of | calcium oxylate and calcium phosphate
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| other sources of calculi | Mg, NH4-PO4, urice acid, cystine
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| 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
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| how does calculi form | forms around a nidus, becomes trapped and accumulates other crystals
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| where do calculi appear | they appear in renal tubules, calcyes, pelvis, ureters, bladder
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| clinical manifestations of calculi | pain (renal colic flank/groin), n/v, hematuria, bacteriuria
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| treatment of calculi | deal with pain first, then stone passage, prevent new stones
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| s/s cystitis (bladder inf/UTI) | frequency/urgency/dysuria --- suprapubic/flank/low pack pain ---
hematuria, cloudy urine ---10% asymptomatic/30% no bacteria in urine
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| UTI definition | infection of any structure in urinary tract - caused by baceteria
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| C & S will be positive UTI if these bacteria present | Gram - E.Coli, Proteus, Pseudomonas.
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| less common microbes in UTI | staphylococcus, candida/fungi in immunosuppressed
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| what is cystitis | inflammation of bladder due to UTI.
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| 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
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| What is pyelonephritis | differs from simple UTI as it occurs proximal to bladder in ureters, or renal pelvis/interstitium.
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| How does pyelonephritis present | presents either unilateral or bilateral, more common in woman with same G- bugs - primarily E.Coli (proteus, pseudomonas)
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| what are risk factors for acute pyelonephritis | renal calculi, vesicourethral reflux (urine backs up bringing bacteria), pg, neurogenic baldder, instrumentation, sexual trauma
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| do we find acute pyelonephritis in the glomeruli | no, only kidney (tubules, pelvis, calyces, medulla) and book says in ureters
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| pathophys of pyelonephritis | infection --> inflamm process that is FOCAL AND IRREGULAR --> medulla infiltrated with WBCs (glomeruli not effected)--> purulent urine/abcess/necrosis
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| acute pyelonephritis - bacterial count and does it cause renal failure | bacteria count decreases until urine is sterile, rarely causes renal failaur
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| clinical manifistations - treat with Antibiotics - of acute pyelonephritis | fever/chills. flank/groin pain. frequency/dysuria. costovertebral tenderness. children/elderly show nonspecific fever, malaise
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| causes of chronic pyelonephritis | caused by persistent/recurrent autoimmune process, NSAIDs, ischemia, radiation. Also may due to calculi or ureteral reflux
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| does chronic pyelonphritic lead to renal failure | yes, Yes, YES it CAN lead to renal faire!
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| pathophys of chronic pyelonephritis | chronic obstruction/inf/inflamm --> atrophy in renal pelvis/calyces --> tubules destroyed --> can't concentrate urine -->chronic renal failure
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| clinical manifestations of pyelonephritis | can't conserve Na yet HTN, hyperkalemia, metab acidosis, dehydration/dilute urine. frequency/dysuria/flank pain
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| When does fever present - lower UTI or pyelonephritis | fever presents with pyelonephritis
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| glomerulonephritis is inflamm of glomerulus caused by | caused by immunologic abnormalities, drugs, toxins, ROS, vascular disorders, systemic diseases
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| what is MOST COMMON CAUSE of chronic and end-stage renal failure | glomerulonephritis is most common cause
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| 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)
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| 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
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| clinical manifestations of glomerulonephritis | hematuria/RBC casts---protenuria---DECREASED GFR---oliguria---ECF edema---HTN
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| define renal insufficiency | down to 25% of normal GFR (25/30 ml/min)
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| define renal failure | GFR decreased to 10-25% of normal
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| define ESRF end-stage renal failure | less than 10% of renal function remains
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| 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
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| What is acute prerenal failure | not enough blood going to glomerulus --> decreased GFR --> acute tubular necrosis or cortical necrosis
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| 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)
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| what causes decreased renal blood flow/poor perfusion seen in prerenal acute RF | vasocon, hypoTN, hypovolemia, hemorrhage, inadequate CO
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| what is most common type of renal failure | intrarenal RF is most common type, affects the kidney itself
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| What causes intrarenal acute RF | ATN = acute tubular necrosis bwo ischemia/ROS --cellular injury/swelling/necrosis.
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| kidney/nephron surgery, nephrotoxic drugs, xray media associated with what type of RF | associated with intrarenal acute RF
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| TN or ATN (tubular necrosis) generally associated with this underlying condition | usually associated with ischemia
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| what is postrenal acute RF | usually occurs after kidney bwo urinary tract obstruction & edema of tubular lumen - - - affects kidneys bilaterally
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| manifestations of postrenal acute RF | hours of anuria - flank pain - polyuria.
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| pts DO recover from ACUTE renal failure by these clinic progressions | oliguria - diuresis -recovery to normal function
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| 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
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| what are the UREMIC/UREMIA symptoms seen in chronic renal failure | anorexia/wt loss --- n/v/d/c ---itching---edema---neuro changes
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| 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
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| lab/diagnostic indicators of chronic RF | high Pcr, high BUN, small kidney size, biopsy confirms diagnosis
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| 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
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| pts with chronic renal failure have | liver AND kidney problems --> coagulation problems --> prolonged coagulation bwo platelet dysfunction at vascular endothelial junction
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| what is azotemia | bnormally high levels of nitrogen-containing compounds, such as urea, creatinine, various body waste, etc. generally found in all renal failures
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