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88 Cards in this Set
- Front
- Back
Kidney Functions
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1.Reabsorption of water, electrolytes, all glucose, amino acids, proteins and vitamins.
2.Aids with acid base balance-excretes bicarb 3.Removal of waste from blood and formation of urine. 4. Secretion of hormones Erythropoietin- needed for RBC formation Renin-RAS- Renin Aldosterone System Vitamin D |
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What is found in the
Cortex Medulla |
Cortex: Contains all glomeruli+85% of nephron tubules. Juxtamedullary nephrons
Medulla: Tubules, ducts, Loop of Henle |
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Function of
GLOMERULUS (found in cortex) TUBULE (found in medulla) |
GLOMERULUS (found in cortex)
forms a protein-free filtrate from blood TUBULE (found in medulla) processes the filtrate to form urine |
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Sympathetic innervation of kidney results in
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Stimulation of SNS results in renal vasoconstriction and renin release.
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1. The main driving force for filtration is
2. The most important physiologic regulator of GFR is |
1. hydrostatic pressure in the glomerular capillaries.
2. blood volume. Increased fluid intake increases blood volume increasing B/P slightly increasing GFR. |
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How are glomerular capillaries protected from fluctuations in B/P
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by autoregulation
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What does the body do in response to a drop in blood pressure? (which accompanies the loss of fluid)
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1. triggers the hypothalamus to rapidly release ADH from post pituitary
2. ADH increases water reabsorption by the kidney by increasing water permeability of the distal tubules and collecting ducts 3. each juxtaglomerular apparatus which responds by secreting renin 4. This triggers the formation of angiotensin II which stimulates release of aldosterone from the adrenal cortex thus slowly boosting water reabsorption by the kidneys by increasing reabsorption of Na, and thus water |
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glomerular filtrate contains
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everything but large molecules such as proteins, contains ions, urea, glucose, minerals, vit, some drugs
99% is actively reabsorbed |
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nephraglia manifests as
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CVA tenderness
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Kidney Disease manifests as
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nephraglia
Abnormal Urinalysis Abnormal findings in: KUB, US, CT, MRI, Biopsy |
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Intrarenal disorder: Infection is caused by
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1. Hostile environment: Intrarenal: pH, urea
Postrenal: prostatic secretions and glands in women secrete mucous 2. Unidirectional flow- back flow causes damage 3. Epithelial cells trap bacteria for inflammatory mediators to kill bacteria: |
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Kidney infection presents what symptoms?
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Thus, pain, urgency, frequency
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What populations are at risk for kidney infection
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Premature newborns
Children Sexually active and pregnant women Women on certain Antibiotics Older women Diabetics Think of diabetes as chronic inflammatory disease Indwelling catheters |
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Acute Pyelonephritis
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Infection of renal pelvis and interstitium
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Etiology Acute Pyelonephritis
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Pregnancy major risk factor- due to chg hormones-look on dip stick for protein in urine
DM- diabetes Vesicoureteral reflux esp children- urine going back into kidney, congenital malformation E. Coli in 80% of acute cases |
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What is causing Acute Pyelonephritis
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Ascending bacteria along the ureters may enter via bloodstream
Epithelial cells trap bacteria for inflammatory mediators to kill bacteria- sticky bomb Inflammatory chemokines=leukocytes + inflammatory mediators=parenchymal damage. |
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What s/s presents with Acute Pyelonephritis
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Fever, chills; Urosepsis
UTI s/s frequency, urgency and pain on urination. CVA tenderness |
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How is Acute Pyelonephritis diagnosed?
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Urinalysis=significant bacteria
RBC, WBC(+casts), nitrates, proteinuria |
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Treatment for Acute Pyelonephritis
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ABX 7-10 days
urine culture if w/o improvement in 48 hrs |
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What do you look for in children when you can’t tell frequency or pain
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Look for Fever, chills
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Normal specific gravity of urine
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1.003-1.030
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What is the etiology of Chronic Pyelonephritis
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1. Recurring or inadequately managed infections
2. Inflammation and scarring of tissue 3. Acute may lead to chronic 4. Often associated with chronic obstruction 5. At Risk Individuals such as those with obstructive disorders i.e. renal calculi (stones), neurogenic bladder, vesicoureteral reflux or Intrarenal disease |
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Chronic Pyelonephritis can lead to
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renal failure
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What is vesicoureteral reflux –
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urine goes back up to kidney
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Early sx of Chronic Pyelonephritis can often be minimal and may include __________.
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HTN, due to renin
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Dx Chronic Pyelonephritis :
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IV pyelogram & ultrasound
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Urinary Tract Obstruction can be caused by
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Congenital
Stones Tumors Trauma Edema Pregnancy BPH |
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which of the 3 is most dangerous? Calyceal stone, renal pelvic stone, upper ureter stone
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upper ureter stone, can kill you because ureter is blocked off
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Complications of obstruction:
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Infection, sepsis, acute renal failure and ?CKD chronic kidney disease
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Hydroureter-
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complete obstruction of ureter, renal pelvis and tubules enlarge
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Hydronephrosis-
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enlarged kidney
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Manifestations of renal obstructions:
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Wt gain, nausea, malaise, headaches, LE edema
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Renal Calculi Nephrolithiasis
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kidney stones
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most common Nephrolithiasis
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calcium oxalate most common
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contributors of renal calculi
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Contributors:
High pH in urine – alkaline. Bacteria split NH3 Uric acid - gout Prolonged immobilization Purine diets – organ meats Increased BMI, change from a person’s normal |
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If you find calcium in stone, this could indicate problems in the
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parathyroid
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presentations of renal calculi
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Presents with acute pain:
may be flank, CVA, testicles or labia n/v, hematuria, elevated VS |
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Diagnosis renal calculi
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Diagnosis
CT, UA for pH, CBC, BUN/Creatinine; dietary history, family history, medications |
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treatment renal calculi
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Treatment:
pain relief and prevention; maybe surgical removal of the stone. Ultrasonic or laser lithotripsy. |
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Glomerular Disorders
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Immune or inflammatory most often implicated- is responsible for it
Proteinuria is classically the clinical manifestation |
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Classification r/t degree of proteinuria:
Nephrotic syndrome Nephrosis Nephritic syndrome |
Nephrotic syndrome >3to 3.5 gm/24 hrs
Nephrosis 2 gm/24 hrs Nephritic syndrome mild proteinuria |
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Glomerulonephritis
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Inflammation of glomerulus and surrounding tissue
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Inflammation of glomerulus and surrounding tissue r/t
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drugs
Toxins vascular disorder systemic diseases-DM, HTN immunologic issues |
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Leading cause of chronic and end stage renal failure
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Glomerulonephritis
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Pediatric etiology of glomerulonephritis
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β-hemolytic Streptococci
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Clinical manifestations of glomerulonephritis
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Hematuria-smoky urine
Edema r/t decreased GFR Proteinuria Oliguria- absence of urine Hypertension- renin stimulated Reduced complement levels due to infection |
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What is responsible for manifestations of glomerulonephritis
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Capillaries are leaking
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Chronic Glomerulonephritis results from
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Several years of proteinuria and hematuria but no other symptoms
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Chronic Glomerulonephritis causes what changes in kidney?
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Fibrotic changes with tubular dilation and atrophy may develop.
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Chronic Glomerulonephritis is associated with
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Associated with hypercholesterolemia, IDDM type I, and SLE
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Three types of immune mechanism influencing renal disease
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1. Antigen – antibody
2. Antibodies against basement membrane 3. Streptococcal release of altering enzyme β-hemolytic Streptococci |
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What effect does the immune response have on kidney which leads to renal failure
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All alter membrane permeability and increase swelling, decreasing blood flow and filtration
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What lab tests are abnormal with renal damage
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Elevated serum Creatinine and BUN
Proteinuria and hematuria, casts Renal biopsy determines extent of injury and type. |
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Treatment for renal damage
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consists of correcting underlying cause, and controlling for:
HTN, edema, hyperkalemia, hyperlipidemia |
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Problems associated with Renal Disease
Calcium loss Anemia |
decreased Ca stimulates PTH, Stimulated PTH causes release of calcium from the bone and enhanced urinary excretion of phophate. Overtime with decreased GFR less phosphate is excreted, and now increases, thus hyperphosphtemia and hypocalcemia and bone disease are acclerated
inadequate production of erythropoietin, Decreased RBCS life span |
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Problems associated with Renal Disease
Lipids Protein loss |
the ratio of LDL to HDL goes to LDL and an accelerated atherosclerosis occurs
Proteinuria and a negative nitrogen balance, but need to restrict dietary protein to preserve GFR |
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Problems associated with Renal Disease
Acid Base Hyperkalemia |
develop a acidotic state
increased plasma levels with progressive decrease of GFR |
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Pathophysiology Renal Disease and HTN
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1. Released renin enzyme in response to the increased pressure in the renal vascular
2. Converts angiotension I to angiotension II 3. Vasoconstriction and increased arterial pressure 4. Increased aldosterone secretion 5. Systemic hypertension 6. Primary medication treatment: ACE inhibitors |
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Primary medication treatment for HTN due to renal disease
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ACE inhibitors
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ACE inhibitors:
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BLOCKS ANGIOTENSION I CONVERTING TO ANGIOTENSION II
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In order for the kidney to function properly it requires:
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Normal renal blood flow: RBF
Functioning Glomeruli: GFR Functioning Tubules Clear Urinary Outflow tract for drainage and elimination of urine formed from body’s waste |
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What allows for the maintenance of a near normal Intrarenal hemodynamic environment (RBF, RPF, GFR and FF ) despite changes in the systemic blood pressure
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autoregulation
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Interruption of renal function has significant ramifications where?
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every body system
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Comorbidities with kidney disease:
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preexisting kidney conditions, HTN, DM, CHF, liver impairment/failure
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Elderly and problems with kidneys
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Autoregulation, concentrating urine, ADH/ thirst, K+, GFR.
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Oliguria
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<400 ml/24 hrs
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Anuria
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<100 ml/24 hrs
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Azotemia
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ALL METABOLITES ARE STAYING IN BODY
silent found by changes in BUN |
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Uremia
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symptomatic, causes death
toxic condition of retention of waste products clinical syndrome associated with fluid, electrolyte, and hormone imbalances and metabolic abnormalities |
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Prerenal acute renal failure due to
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diminished perfusion of kidney due to
1.volume deficits due to fever, vomiting, diarrhea, burns, hemorrhage, overuse of diuretic 2.heart cannot generate output, CHF 3. vascular autoregulation interfered by ACE inhibitors, COX inhibitors, angiotension II receptor blocker, NSAIDS 4. nephrotic syndrome- mild protein loss due to gromular inflammation 5. hypercalcemia 6. thrombosis, embolus, dissection, stenosis |
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What needs to be in balance for intrarenal autoregulation?
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vasodilatation and vasoconstriction
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what causes vasodilation?
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PG, Kinines, ANP, NO
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what causes vasoconstriction?
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Renin, All, ADH
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influence of intrarenal constriction of afferent arterioles on GFR
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loss of GFR
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Area involved in intrarenal Acute Renal Failure:
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vasculature, interstitial, glomerular or tubular
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most common cause of ARF Acute Renal Failure
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Acute tubular necrosis (ATN)
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Acute tubular necrosis (ATN) is a result of
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caused by prerenal ischemia
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ATN may lead to
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ESCRD, end stage chronic renal disease
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Ischemia + inflammatory response leads to
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Acute tubular necrosis
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Acute Renal Failure: Post Renal
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due to obstruction
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intraluminal intrinsic causes of post renal ARF
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stone, blood clot, papillary nec
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intramural intrinsic obstruction causes
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BPH, ureter stricture, carcinoma prostate, bladder tumor, radiation fibrosis
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extrinsic causes of ARF, post renal
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pelvic malignancies
prolapsed uterus |
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Stages of ATN , acute tubular necrosis
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Oliguria stage
Diuretic stage Recovery stage |
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describe oliguria stage
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urine output drops=hypervolemia, THN, JVD
Metabolic wastes retained Hyperkalemia, fluid electrolyte imbalance uremic syndrome |
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Describe diuretic stage
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polyuria due to concentrating mechanism not recovered
volume deficit elevated BUN continues hypokalemia |
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describe recover stage
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full renal function recovered, serum creatine normal
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why does kidney disease cause anemia?
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kidneys don't manufacture erythropoietin
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